Product Citations: 251

Fig.2.F showing Western Blotting from the publication: A positive feedback loop between ZEB2 and ACSL4 regulates lipid metabolism to promote breast cancer metastasis.
Fig.5.C showing Western Blotting from the publication: Catalytic antibodies in arrhythmogenic cardiomyopathy patients cleave desmoglein 2 and N-cadherin and impair cardiomyocyte cohesion.
Fig.7.F showing Western Blotting from the publication: Ladinin 1 Shortens Survival via Promoting Proliferation and Enhancing Invasiveness in Lung Adenocarcinoma.
Fig.1.F showing Western Blotting in a Homo sapiens (Human) sample from the publication: m6A RNA methylation regulates the transcription factors JUN and JUNB in TGF-β-induced epithelial-mesenchymal transition of lung cancer cells.
Fig.4.E showing Western Blotting from the publication: Loss of MEN1 leads to renal fibrosis and decreases HGF-Adamts5 pathway activity via an epigenetic mechanism.
Fig.4.F showing Western Blotting from the publication: Loss of MEN1 leads to renal fibrosis and decreases HGF-Adamts5 pathway activity via an epigenetic mechanism.
Fig.5.E showing Western Blotting from the publication: Loss of MEN1 leads to renal fibrosis and decreases HGF-Adamts5 pathway activity via an epigenetic mechanism.
Fig.5.G showing Western Blotting in a Homo sapiens (Human) sample from the publication: Epstein-Barr virus-encoded microRNA BART22 serves as novel biomarkers and drives malignant transformation of nasopharyngeal carcinoma.
Fig.4.H showing Western Blotting in a Homo sapiens (Human) sample from the publication: Epstein-Barr virus-encoded microRNA BART22 serves as novel biomarkers and drives malignant transformation of nasopharyngeal carcinoma.
Fig.6.G showing Western Blotting in a Homo sapiens (Human) sample from the publication: Epstein-Barr virus-encoded microRNA BART22 serves as novel biomarkers and drives malignant transformation of nasopharyngeal carcinoma.
Fig.7.J showing Western Blotting in a Homo sapiens (Human) sample from the publication: Epstein-Barr virus-encoded microRNA BART22 serves as novel biomarkers and drives malignant transformation of nasopharyngeal carcinoma.
Fig.3.B showing Western Blotting in a Homo sapiens (Human) sample from the publication: PGC1α Cooperates with FOXA1 to Regulate Epithelial Mesenchymal Transition through the TCF4-TWIST1.
Fig.3.F showing Western Blotting in a Homo sapiens (Human) sample from the publication: PGC1α Cooperates with FOXA1 to Regulate Epithelial Mesenchymal Transition through the TCF4-TWIST1.
Fig.5.B showing Western Blotting in a Homo sapiens (Human) sample from the publication: PGC1α Cooperates with FOXA1 to Regulate Epithelial Mesenchymal Transition through the TCF4-TWIST1.
Fig.7.C showing Western Blotting from the publication: Downregulated ADAMTS1 Incorporating A2M Contributes to Tumorigenesis and Alters Tumor Immune Microenvironment in Lung Adenocarcinoma.
Fig.4.B showing Western Blotting from the publication: Upregulation of PEDF Predicts a Poor Prognosis and Promotes Esophageal Squamous Cell Carcinoma Progression by Modulating the MAPK/ERK Signaling Pathway.
Fig.5.B showing Western Blotting from the publication: Upregulation of PEDF Predicts a Poor Prognosis and Promotes Esophageal Squamous Cell Carcinoma Progression by Modulating the MAPK/ERK Signaling Pathway.
Fig.1.F showing Western Blotting from the publication: Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy.
Fig.1.A showing Western Blotting from the publication: Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy.
Fig.1.B showing Western Blotting from the publication: Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy.
Fig.1.E showing Western Blotting from the publication: Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy.
Fig.1.A showing Western Blotting from the publication: Targeting endothelin 1 receptor-miR-200b/c-ZEB1 circuitry blunts metastatic progression in ovarian cancer.
Fig.6.B showing Western Blotting from the publication: Targeting endothelin 1 receptor-miR-200b/c-ZEB1 circuitry blunts metastatic progression in ovarian cancer.
Fig.3.B showing Western Blotting from the publication: Targeting the TGFβ pathway in uterine carcinosarcoma.
Fig.4.E showing Western Blotting from the publication: Targeting the TGFβ pathway in uterine carcinosarcoma.
60 images found

PCK2 promotes invasion and epithelial-to-mesenchymal transition in triple-negative breast cancer by promoting TGF-β/SMAD3 signaling through inhibiting TRIM67-mediated SMAD3 ubiquitination.

In Cancer Biology & Therapy on 1 December 2025 by Chang, T. M., Fang, W. Y., et al.

PCK2, which encodes mitochondrial phosphoenolpyruvate carboxykinase (PEPCK-M), is upregulated in various cancers. We demonstrated high expression of PEPCK-M in approximately half of triple-negative breast cancers (TNBCs) previously. TNBC is associated with an aggressive phenotype and a high metastasis rate. In this study, we investigated the role of PCK2 in TNBC. PCK2 knockdown suppressed proliferation and mTOR signaling in TNBC cells. In addition, cell invasion/migration ability and the expression of epithelial-to-mesenchymal transition (EMT) markers were positively correlated with PCK2 expression in TNBC cells via regulation of transforming growth factor-β (TGF-β)/SMAD3 signaling. SMAD3 was positively regulated by PCK2 in TNBC cells. Knockdown of SMAD3 in PCK2-overexpressing TNBC cells reduced the expression levels of EMT markers, Snail and Slug, and suppressed cell invasion/migration. In addition, PCK2 knockdown attenuated the stimulatory effect of TGF-β on SMAD3 phosphorylation in TNBC cells. PEPCK-M promotes the protein and mRNA expression of SMAD3 via competitive binding to tripartite motif-containing 67 (TRIM67), an E3 ubiquitin ligase, to reduce SMAD3 ubiquitination, which leads to promoting nuclear translocation of SMAD3 and autoregulation of SMAD3 transcription. Moreover, high PCK2 mRNA expression was significantly associated with poor survival in TNBC patients. In conclusion, our study revealed for the first time that PCK2 activates TGF-β/SMAD3 signaling by regulating the expression and phosphorylation of SMAD3 by inhibiting TRIM67-mediated SMAD3 ubiquitination and promoting the stimulatory effect of TGF-β to promote TNBC invasion. The regulatory effect of PCK2 on mTOR and TGF-β/SMAD3 signaling suggests that PCK2 is a potential therapeutic target for suppressing TNBC progression.

  • WB
  • Cancer Research
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Phospholipase D6 activates Wnt/β-catenin signaling through mitochondrial metabolic reprogramming to promote tumorigenesis in colorectal cancer.

In Experimental & Molecular Medicine on 21 April 2025 by Lee, H. J., Lim, S. H., et al.

Phospholipase D6 (PLD6) is a critical enzyme involved in mitochondrial fusion with a key role in spermatogenesis. However, the role of PLD6 in cancer remains unknown. Notably, Wnt signaling, energy metabolism and mitochondrial function show complex interactions in colorectal cancer (CRC) progression. Here we found that PLD6 is highly expressed in CRC and positively correlated with poor prognosis. We present a novel function of PLD6 in activating Wnt/β-catenin signaling by enhancing mitochondrial metabolism. PLD6 depletion suppresses the oncogenic properties of CRC cells and impairs mitochondrial respiration, leading to reduced mitochondrial length, membrane potential, calcium levels and reactive oxygen species. PLD6 depletion also disrupts mitochondrial metabolic reprogramming by inhibiting the tricarboxylic acid cycle and mitochondrial oxidative phosphorylation, resulting in altered intracellular levels of citrate and acetyl-CoA-both key modulators of Wnt/β-catenin activation. PLD6-mediated acetyl-CoA production enhances β-catenin stability by promoting its acetylation via the acetyltransferases CREB-binding protein and P300/CREB-binding-protein-associated factor. Consequently, PLD6 ablation reduces cancer stem cell-associated gene expression downstream of Wnt/β-catenin signaling, suppressing stem-like traits and chemoresistance to 5-fluorouracil. Furthermore, PLD6 depletion attenuates CRC tumorigenesis in both subcutaneous and orthotopic tumor models. Overall, PLD6 acts as an oncogenic switch by promoting mitochondria-mediated retrograde signaling, thereby regulating Wnt signaling in CRC.
© 2025. The Author(s).

  • Biochemistry and Molecular biology
  • Cancer Research
  • Cell Biology
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MSK1 promotes colorectal cancer metastasis by increasing Snail protein stability through USP5-mediated Snail deubiquitination.

In Experimental & Molecular Medicine on 1 April 2025 by Hong, K. S., Ryu, K. J., et al.

Mitogen- and stress-activated protein kinase 1 (MSK1), a Ser/Thr kinase, phosphorylates nuclear proteins to increase their stability and DNA-binding affinity. Despite the role of MSK1 in promoting cancer progression in colorectal cancer (CRC), the precise molecular mechanisms remain unelucidated. Here we show that MSK1 expression induces the epithelial-mesenchymal transition (EMT) process and increases CRC cell metastasis. Furthermore, we discovered that MSK1 interacts with Snail, a key EMT regulator, and increases its stability by inhibiting ubiquitin-mediated proteasomal degradation. Importantly, MSK1 increased Snail protein stability by promoting deubiquitination rather than inhibiting its ubiquitination. Finally, we identified USP5 as an essential deubiquitinase that binds to Snail protein phosphorylated by MSK1. Based on the experimental data, in CRC, MSK1-Snail-USP5 axis can promote EMT and metastasis of CRC. Together, our findings provide potential biomarkers and novel therapeutic targets for further research in CRC.
© 2025. The Author(s).

  • Biochemistry and Molecular biology
  • Cancer Research
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Transcriptional landscape and predictive potential of long noncoding RNAs in peritoneal recurrence of gastric cancer.

In Molecular Cancer on 30 December 2024 by Cai, X. X., Chen, G. M., et al.

Long noncoding RNAs (lncRNAs) play a critical role in gastric cancer (GC) progression and metastasis. However, research comprehensively exploring tissue-derived lncRNAs for predicting peritoneal recurrence in patients with GC remains limited. This study aims to investigate the transcriptional landscape of lncRNAs in GC with peritoneal metastasis (PM) and to develop an integrated lncRNA-based score to predict peritoneal recurrence in patients with GC after radical gastrectomy.
We analyzed the transcriptome profile of lncRNAs in paired peritoneal, primary gastric tumor, and normal tissue specimens from 12 patients with GC in the Sun Yat-sen University Cancer Center (SYSUCC) discovery cohort. Key lncRNAs were identified via interactive analysis with the TCGA database and SYSUCC validation cohort. A score model was constructed using the LASSO regression model and nomogram COX regression and evaluated using receiver operating characteristic curves. The role of lncRNAs in the PM of GC was then examined through wound healing, Transwell, 3D multicellular tumor spheroid invasion, and peritoneal cavity xenograft tumorigenicity assays in mice.
Five essential lncRNAs were screened and incorporated into the PM risk score to predict peritoneal recurrence-free survival (pRFS). We developed a comprehensive, integrated nomogram score, including the PM risk score, pT, pN, and tumor size, which could effectively predict the 5-year pRFS with an Area under the curve of 0.79 (95% CI: 0.71-0.88). Subsequently, we demonstrated that one of these lncRNAs, CASC15, promoted the invasion and migration of GC cells in vitro and facilitated the PM of GC cells in vivo, initially verifying that lncRNAs contribute to the PM of GC. Mechanistic analysis demonstrated that CASC15 promoted EMT and metastasis by activating the JNK and p38 pathways.
A lncRNA-based integrated score was constructed in this study to predict peritoneal recurrence in patients clinically.
© 2024. The Author(s).

  • WB
  • Homo sapiens (Human)
  • Biochemistry and Molecular biology
  • Cancer Research
  • Genetics
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Vinculin Y822 phosphorylation regulates cardiomyocyte adhesion dynamics and adherens junction maturation in the heart

Preprint on BioRxiv : the Preprint Server for Biology on 3 November 2024 by Li, X., Wortelboer, R., et al.

In the heart, cell-matrix and cell-cell adhesions reorganize in response to increased cardiac demand and growth to promote cardiomyocyte maturation. Vinculin, a mechanosensitive adaptor protein, links filamentous actin to cell-matrix and cell-cell adhesions and is thus positioned to regulate adhesion reorganization. However, how the two adhesion systems are coordinated in the heart, and the role of vinculin in this process is poorly understood. Here, we define the role of vinculin phosphorylation at tyrosine residue 822 (pY822) in cardiomyocyte adhesion and heart function. We found that pY822 correlated with dynamic junction remodeling in the developing heart but was lost as junctions matured postnatally. We then mutated Y822 to phenylalanine (Y822F) in the mouse to determine pY822 function in vivo. Homozygous mutant Vcl Y822F mice were viable and exhibited normal cardiac function at ten weeks of age; however, cardiac dysfunction was observed at 28 weeks. Vinculin and adherens junction proteins were reduced at cardiomyocyte junctions in Y822F hearts. In contrast, α5/β1 integrin and fibronectin increased along the lateral border of Y822F cardiomyocytes. Our results demonstrate that vinculin Y822 phosphorylation regulates the balance between cadherin and integrin adhesion organization, highlighting the importance of post-translational modification in modulating vinculin function in heart physiology.

  • Mus musculus (House mouse)
  • Cardiovascular biology
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A positive feedback loop between ZEB2 and ACSL4 regulates lipid metabolism to promote breast cancer metastasis.

In Elife on 11 December 2023 by Lin, J., Zhang, P., et al.

Fig.2.F
Fig.2.F showing Western Blotting from the publication: A positive feedback loop between ZEB2 and ACSL4 regulates lipid metabolism to promote breast cancer metastasis.
  • WB
Overexpression of ACSL4 contributes to ZEB2-mediated breast cancer invasion.(A) Cell metastatic capacity was analyzed by wound healing assay in control or ACSL4 overexpression MCF-7 cells (left panel). Expression of ACSL4 was analyzed by western blot in control or ACSL4 overexpression MCF-7 cells... more
Overexpression of ACSL4 contributes to ZEB2-mediated breast cancer invasion.(A) Cell metastatic capacity was analyzed by wound healing assay in control or ACSL4 overexpression MCF-7 cells (left panel). Expression of ACSL4 was analyzed by western blot in control or ACSL4 overexpression MCF-7 cells. Quantification of relative migration distance (right panel). Scale bar, 5 mm. (B) Cell invasive capacity was analyzed by transwell invasion assay in control or ACSL4 overexpression MCF-7 cells (left panel). Quantification of relative invasive cells (right panel). Scale bar, 1 mm. (C) Cell metastatic capacity was analyzed by wound healing assays in control or ACSL4 silencing MDA-MD-231 cells (shACSL4) (left panel). Expression of ACSL4 was analyzed by western blot in control or ACSL4 silencing MDA-MD-231 cells (shACSL4). Quantification of relative migration distance (right panel). Scale bar, 5 mm. (D) Cell invasive capacity was analyzed by transwell invasion assay in control or ACSL4 silencing MDA-MD-231 cells (shACSL4) (left panel). Quantification of relative invasive cells (right panel). Scale bar, 1 mm. (E) KEGG (https://www.kegg.jp/) pathway enrichment analysis of differentially expressed genes by RNA-sequencing between control and ACSL4 knockdown MDA-MB-231 cells. The top 10 deferential pathways were listed. (F) Expression of three epithelial–mesenchymal transition (EMT)-related genes, E-cadherin, N-cadherin, and vimentin, was analyzed by western blotting in control, ACSL4, or ZEB2-silencing MDA-MB-231 cells. (G) Cell invasive and metastatic capacities were analyzed by transwell invasion assay and wound healing assays (scale bar, 1/5 mm) in control and ZEB2 knockdown, or ZEB2 knockdown cells that overexpress ACSL4. (H) Protein expression was analyzed by western blot in control, ZEB2 knockdown (shZEB2), and ZEB2 knockdown with ACSL4 overexpression (shZEB2 + ACSL4) cells. (I) Quantification of relative invasive cells in G. (J) Quantification of relative migration distance in G. Graphs indicated the statistical analysis in G analyzed by Student’s t-test (mean ± standard error of the mean [SEM]). **p < 0.01, ***p < 0.001, ****p < 0.0001. All results are from three or four independent experiments.Figure 2—source data 1.The datasets of differentially expressed genes by RNA-sequencing between control and ACSL4 knockdown MDA-MB-231 cells.Figure 2—source data 2.The raw unedited gels or blots images of Figure 2.The datasets of differentially expressed genes by RNA-sequencing between control and ACSL4 knockdown MDA-MB-231 cells.The raw unedited gels or blots images of Figure 2.Fluorescence staining of Phalloidin in control or ACSL4 knockdown MDA-MB-231 cells.The morphology of cells was analyzed by the ratio of length to width (right panel). ***p < 0.001.ZEB2 increases the metastatic and invasive capacities in breast cancer cells.(A) Cell metastatic capacity was analyzed by wound healing assay in control or ZEB2 overexpression MCF-7 cells (left panel). Quantification of relative migration distance (right panel). Scale bar, 5 mm. (B) Cell invasive capacity was analyzed by transwell invasion assay in control or ZEB2 overexpression MCF-7 cells (left panel). Quantification of relative invasive cells (right panel). Scale bar, 1 mm. (C) Wound healing assays were performed in control cells or ZEB2 knockdown (shZEB2) MDA-MD-231 cells (left panel). Quantification of relative migration distance (right panel). Scale bar, 5 mm. (D) Transwell invasive assay was performed in control cells or ZEB2 knockdown (shZEB2) MDA-MD-231 cells (left panel). Quantification of relative invasive cells (right panel). Scale bar, 1 mm. **p < 0.01, ***p < 0.001, ****p < 0.0001. less

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Catalytic antibodies in arrhythmogenic cardiomyopathy patients cleave desmoglein 2 and N-cadherin and impair cardiomyocyte cohesion.

In Cell Mol Life Sci on 14 July 2023 by Yeruva, S., Stangner, K., et al.

Fig.5.C
Fig.5.C showing Western Blotting from the publication: Catalytic antibodies in arrhythmogenic cardiomyopathy patients cleave desmoglein 2 and N-cadherin and impair cardiomyocyte cohesion.
  • WB
Protein expression analysis and dissociation assays in HL-1 cells treated with AC-IgGs. A Western blot of lysates prepared from HL-1 cells treated with respective IgGs for 24 h. B Western blot quantification of pp38MAPK for the blots shown in A. Ratio between pp38MAPK and total p38MAPK was normal... more
Protein expression analysis and dissociation assays in HL-1 cells treated with AC-IgGs. A Western blot of lysates prepared from HL-1 cells treated with respective IgGs for 24 h. B Western blot quantification of pp38MAPK for the blots shown in A. Ratio between pp38MAPK and total p38MAPK was normalized to healthy control IgG (IgG), and means represents ± SEM. N = 3–4. C Western blots of Triton-X-100 lysates prepared after incubating HL-1 cells with mentioned IgG samples for 24 h. A supernatant fraction represents non-cytoskeleton bound proteins, and a pellet fraction represents cytoskeleton bound proteins. F/R (Forskolin/Rolipram) treatments served as a positive experimental control for the activation of p38MAPK. D Western blot quantification of pp38MAPK in the supernatant fractions of the blots shown in B. Ratio between pp38MAPK and total p38MAPK was normalized to IgG-control (IgG), and means represents ± SEM. N = 4–6. *Indicates p < 0.05, **indicates p < 0.005 compared to healthy control IgGs (IgG); #indicates p < 0.05 compared to control (Ctrl) and NS is not significant. One-way ANOVA with Holm–Šídák's multiple comparisons test was performed between IgG samples, and a Student’s t-test was performed between control and F/R. E Dissociation assays with HL-1 cells were treated in the presence or absence of 100 µM SB2021890 (SB20), which was added 30 min before 24 h treatment with AC patient IgGs. Data represent the mean ± SEM. N = 4. *Indicates p < 0.05, SB20 compared to vehicle (DMSO) treatment. Multiple unpaired t-tests with Welch correction were performed less

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Ladinin 1 Shortens Survival via Promoting Proliferation and Enhancing Invasiveness in Lung Adenocarcinoma.

In Int J Mol Sci on 27 December 2022 by Chang, C. Y., Huang, Y. C., et al.

Fig.7.F
Fig.7.F showing Western Blotting from the publication: Ladinin 1 Shortens Survival via Promoting Proliferation and Enhancing Invasiveness in Lung Adenocarcinoma.
  • WB
Functional analysis of LAD1 in LUAD. (A) Knockdown efficiency of LAD1 via siRNA method. (B) Cell proliferation is counted when LAD1 expression was downregulated with in A549 and CL1-0 LUAD cancer cell lines. (C) Cell cycle associated proteins are analyzed by Western blot. (D) Cell cycle analysis ... more
Functional analysis of LAD1 in LUAD. (A) Knockdown efficiency of LAD1 via siRNA method. (B) Cell proliferation is counted when LAD1 expression was downregulated with in A549 and CL1-0 LUAD cancer cell lines. (C) Cell cycle associated proteins are analyzed by Western blot. (D) Cell cycle analysis using a flow cytometry. (E) Cell migration in LAD1 knockdown A549 and CL1-0 cell line is assessed by wound-healing assay. (F) Epithelial mesenchymal transition (EMT) markers are also evaluated with Western blot. Both A549 and CL1-0 LUAD cancer cell lines are transfected with control siRNA or LAD1 siRNA. All experiments were performed independently at least three times. (*, p < 0.05; **, p < 0.01; ***, p < 0.005; ****, p < 0.001). less

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m6A RNA methylation regulates the transcription factors JUN and JUNB in TGF-β-induced epithelial-mesenchymal transition of lung cancer cells.

In J Biol Chem on 1 November 2022 by Suphakhong, K., Terashima, M., et al.

Fig.1.F
Fig.1.F showing Western Blotting in a Homo sapiens (Human) sample from the publication: m6A RNA methylation regulates the transcription factors JUN and JUNB in TGF-β-induced epithelial-mesenchymal transition of lung cancer cells.
  • WB
  • Homo sapiens (Human)
Involvement of JUN and JUNB transcription factors in the expression of epithelial and mesenchymal marker genes during TGF-β-induced EMT of A549 lung cancer cells.A, the expression of JUN, JUNB, and JUND mRNAs in TGF-β-induced EMT of A549 cells. QRT–PCR was performed in A549 cells with or without ... more
Involvement of JUN and JUNB transcription factors in the expression of epithelial and mesenchymal marker genes during TGF-β-induced EMT of A549 lung cancer cells.A, the expression of JUN, JUNB, and JUND mRNAs in TGF-β-induced EMT of A549 cells. QRT–PCR was performed in A549 cells with or without TGF-β treatment (∗∗p < 0.01; ns, not significant). B, the expression levels of JUN family proteins in A549 cells. Immunoblotting was performed to detect JUN, JUNB, and JUND proteins in the cells with or without TGF-β treatment. As a control, anti-GAPDH antibody was used to show that equal amounts of proteins were loaded. C–E, the expression of EMT-related marker genes in JUN family knockdown A549 cells. QRT–PCR was performed to detect the expression of CDH1, VIM, FN1, and CDH2 in A549 cells infected with lentivirus-expressing control shRNA or JUN shRNA#1 without or with TGF-β for 24 h (C) (n = 3) (∗∗p < 0.01; ∗p < 0.05; ns, not significant). The similar QRT–PCR results were shown for the knockdown of JUNB (D) and JUND (E) in A549 cells. F and G, knockdown of JUN and JUNB affected the protein expression changes of EMT-related marker genes induced by TGF-β in A549 cells. Immunoblotting of JUN (F), JUNB (G), E-cadherin, vimentin, fibronectin, N-cadherin, and GAPDH proteins was performed using the corresponding antibodies in A549 cells with the knockdown by JUN shRNA#1 (F) and JUNB shRNA#1 (G). EMT, epithelial–mesenchymal transition; QRT–PCR, quantitative RT–PCR; TGF-β, transforming growth factor-beta. less

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Loss of MEN1 leads to renal fibrosis and decreases HGF-Adamts5 pathway activity via an epigenetic mechanism.

In Clin Transl Med on 1 August 2022 by Jin, B., Zhu, J., et al.

Fig.4.E
Fig.4.E showing Western Blotting from the publication: Loss of MEN1 leads to renal fibrosis and decreases HGF-Adamts5 pathway activity via an epigenetic mechanism.
  • WB
Deletion of Men1 induces tubular epithelial‐to‐mesenchymal transition. (A) Scheme of CRISPR/Cas9‐mediated knockout of MEN1 in HK‐2 cells and sgRNA sequence targeting MEN1 CDS exon3. (B) Immunofluorescence staining for F‐actin (red) and 4′, 6′‐diamidino 2‐phenylindole (DAPI, blue) in the MEN1‐WT a... more
Deletion of Men1 induces tubular epithelial‐to‐mesenchymal transition. (A) Scheme of CRISPR/Cas9‐mediated knockout of MEN1 in HK‐2 cells and sgRNA sequence targeting MEN1 CDS exon3. (B) Immunofluorescence staining for F‐actin (red) and 4′, 6′‐diamidino 2‐phenylindole (DAPI, blue) in the MEN1‐WT and MEN1‐KO HK‐2 cells treated with 10‐ng/ml TGF‐β for 48 h; scale bars 10 μm. (C) Immunohistochemistry (IHC) staining for the indicated proteins in the kidney tissues of the Men1f/f and Men1Δ/Δ mice; scale bars 50 μm. (D) Automatic quantification of collagen 1, α‐SMA, E‐cadherin and vimentin IHC staining in kidney tissues of the Men1f/f and Men1Δ/Δ mice (n = 9 mice per group at 8 months, n = 9 mice in the Men1f/f and n = 14 mice in the Men1Δ/Δ groups at 12 months). (E) Western blotting was used to detect the expression of the indicated proteins in the kidney tissues of the Men1f/f and Men1Δ/Δ mice. (F) Western blotting was used to detect the expression of the indicated proteins in the vector‐ and MEN1‐HK‐2 cells after exposure to 10‐ng/ml TGF‐β. (G) Quantification of the greyscale image of indicated proteins in (F) (three biological replicates). The data are represented as mean ± standard deviation (SD);*p < .05, **p < .01, ***p < .001, ****p < .0001. less

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Loss of MEN1 leads to renal fibrosis and decreases HGF-Adamts5 pathway activity via an epigenetic mechanism.

In Clin Transl Med on 1 August 2022 by Jin, B., Zhu, J., et al.

Fig.4.F
Fig.4.F showing Western Blotting from the publication: Loss of MEN1 leads to renal fibrosis and decreases HGF-Adamts5 pathway activity via an epigenetic mechanism.
  • WB
Deletion of Men1 induces tubular epithelial‐to‐mesenchymal transition. (A) Scheme of CRISPR/Cas9‐mediated knockout of MEN1 in HK‐2 cells and sgRNA sequence targeting MEN1 CDS exon3. (B) Immunofluorescence staining for F‐actin (red) and 4′, 6′‐diamidino 2‐phenylindole (DAPI, blue) in the MEN1‐WT a... more
Deletion of Men1 induces tubular epithelial‐to‐mesenchymal transition. (A) Scheme of CRISPR/Cas9‐mediated knockout of MEN1 in HK‐2 cells and sgRNA sequence targeting MEN1 CDS exon3. (B) Immunofluorescence staining for F‐actin (red) and 4′, 6′‐diamidino 2‐phenylindole (DAPI, blue) in the MEN1‐WT and MEN1‐KO HK‐2 cells treated with 10‐ng/ml TGF‐β for 48 h; scale bars 10 μm. (C) Immunohistochemistry (IHC) staining for the indicated proteins in the kidney tissues of the Men1f/f and Men1Δ/Δ mice; scale bars 50 μm. (D) Automatic quantification of collagen 1, α‐SMA, E‐cadherin and vimentin IHC staining in kidney tissues of the Men1f/f and Men1Δ/Δ mice (n = 9 mice per group at 8 months, n = 9 mice in the Men1f/f and n = 14 mice in the Men1Δ/Δ groups at 12 months). (E) Western blotting was used to detect the expression of the indicated proteins in the kidney tissues of the Men1f/f and Men1Δ/Δ mice. (F) Western blotting was used to detect the expression of the indicated proteins in the vector‐ and MEN1‐HK‐2 cells after exposure to 10‐ng/ml TGF‐β. (G) Quantification of the greyscale image of indicated proteins in (F) (three biological replicates). The data are represented as mean ± standard deviation (SD);*p < .05, **p < .01, ***p < .001, ****p < .0001. less

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Loss of MEN1 leads to renal fibrosis and decreases HGF-Adamts5 pathway activity via an epigenetic mechanism.

In Clin Transl Med on 1 August 2022 by Jin, B., Zhu, J., et al.

Fig.5.E
Fig.5.E showing Western Blotting from the publication: Loss of MEN1 leads to renal fibrosis and decreases HGF-Adamts5 pathway activity via an epigenetic mechanism.
  • WB
Menin‐dependent chromatin H3K4me3 modification is involved in regulating epithelial‐to‐mesenchymal transition (EMT). (A) Immunohistochemistry (IHC) staining for H3K4me3 in the kidney tissues of the sham and unilateral ureteral obstruction (UUO) mice 7 days after surgery (n = 8 mice per group); sc... more
Menin‐dependent chromatin H3K4me3 modification is involved in regulating epithelial‐to‐mesenchymal transition (EMT). (A) Immunohistochemistry (IHC) staining for H3K4me3 in the kidney tissues of the sham and unilateral ureteral obstruction (UUO) mice 7 days after surgery (n = 8 mice per group); scale bars 50 μm. (B) IHC staining for H3K4me3 in the kidney tissues of the Men1f/f and Men1Δ/Δ mice at 12 months; scale bars 50 μm. (C and D) Quantification of H3K4me3 IHC staining in (A) and (B), respectively. (E) Western blotting was used to detect the expression of menin in total lysates and modification of the indicated histones in histone extracts in the shLuc‐ and shMEN1‐HK‐2 cells. (F) Mouse renal tubular epithelial cells (mRTECs) were treated with 10‐μM MI‐3 for 2 days before TGF‐β treatment and were collected 2 days after exposure to 10‐ng/ml TGF‐β, and Western blotting was used to detect the expression of the indicated proteins. (G) Western blotting was used to detect the expression of the indicated proteins in the vector‐ and MEN1‐HK‐2 cells 72 h after 10‐μM MI‐3 treatment. (H) Representative morphological image of HK‐2 cells treated with 10‐μM MI‐3 for 72 h; original magnification ×100. (I) Immunofluorescence (IF) staining for F‐actin (red) and DAPI (blue) in the HK‐2 cells treated with 10‐μM MI‐3 for 72 h; scale bars 10 μm. (J) Quantification of the greyscale image of the indicated proteins in (G) (three biological replicates). (K) Integrated genomics view of menin and H3K4me3 chromatin binding at the Has2, Snail and Twist1 gene loci in the kidney tissues of the Men1f/f and Men1Δ/Δ mice at 12 months. The data are represented as the mean ± standard deviation (SD); *p < .05, **p < .01, ***p < .001, ****p < .0001. less

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Epstein-Barr virus-encoded microRNA BART22 serves as novel biomarkers and drives malignant transformation of nasopharyngeal carcinoma.

In Cell Death Dis on 30 July 2022 by Zhang, T., Chen, Z., et al.

Fig.5.G
Fig.5.G showing Western Blotting in a Homo sapiens (Human) sample from the publication: Epstein-Barr virus-encoded microRNA BART22 serves as novel biomarkers and drives malignant transformation of nasopharyngeal carcinoma.
  • WB
  • Homo sapiens (Human)
Overexpression of EBV-miR-BART22 promotes the migration, invasion, and EMT of NPC cells.A The representative image of the distant liver tumor was displayed. *P < 0.05. **P < 0.01. B H&E staining of the spleen tumors (magnification, ×100, Scale bar, 100 μm) were showed. C Representative photomicro... more
Overexpression of EBV-miR-BART22 promotes the migration, invasion, and EMT of NPC cells.A The representative image of the distant liver tumor was displayed. *P < 0.05. **P < 0.01. B H&E staining of the spleen tumors (magnification, ×100, Scale bar, 100 μm) were showed. C Representative photomicrographs of scratch wounds at 0 and 24 h after wounds were made. Scale bar = 100 mm (n = 3 each). Data are means ± S.E.M. *P < 0.05, **P < 0.01. D The C666-1 cellular migration and invasion capability were assessed by transwell migration and Boyden chamber invasion assays (E). Representative micrographs of indicated cells grown on matrigel for 10 days in 3D spheroid invasion assay. F Cells morphology was evaluated by phase-contrast microscopy. G The expression of epithelial and mesenchymal cell markers was examined by WB analysis in EBV-miR-BART-22 inhibition C666-1 and the corresponding control cells. less

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Epstein-Barr virus-encoded microRNA BART22 serves as novel biomarkers and drives malignant transformation of nasopharyngeal carcinoma.

In Cell Death Dis on 30 July 2022 by Zhang, T., Chen, Z., et al.

Fig.4.H
Fig.4.H showing Western Blotting in a Homo sapiens (Human) sample from the publication: Epstein-Barr virus-encoded microRNA BART22 serves as novel biomarkers and drives malignant transformation of nasopharyngeal carcinoma.
  • WB
  • Homo sapiens (Human)
Overexpression of EBV-miR-BART22 promotes the migration, invasion, and EMT of NPC cells.A A representative bright-field image of the livers was shown. Liver weights and metastatic modules number in nude mice that received transplants of indicated cells. Bars correspond to mean ± standard deviatio... more
Overexpression of EBV-miR-BART22 promotes the migration, invasion, and EMT of NPC cells.A A representative bright-field image of the livers was shown. Liver weights and metastatic modules number in nude mice that received transplants of indicated cells. Bars correspond to mean ± standard deviation (SD), **P < 0.01. ***P < 0.001. (B). Representative H&E staining of indicated spleen orthotopic tumors is shown. C CNE-1, CNE-2, and SUNE-1 cells and appropriate controls were used in a wound-healing assay. D Quantification of indicated migrating cells in 5 random fields analyzed by Transwell assays, respectively. E Quantification of indicated invasion cells in 5 random fields analyzed by invasion assays, respectively. F Representative micrographs of indicated cells grown on matrigel for 10 days in 3D spheroid invasion assay. G Cells morphology was evaluated by phase-contrast microscopy. H Expression of epithelial cell marker and mesenchymal cell marker in indicated cells were examined by WB analysis. β-actin was used as a loading control. less

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Epstein-Barr virus-encoded microRNA BART22 serves as novel biomarkers and drives malignant transformation of nasopharyngeal carcinoma.

In Cell Death Dis on 30 July 2022 by Zhang, T., Chen, Z., et al.

Fig.6.G
Fig.6.G showing Western Blotting in a Homo sapiens (Human) sample from the publication: Epstein-Barr virus-encoded microRNA BART22 serves as novel biomarkers and drives malignant transformation of nasopharyngeal carcinoma.
  • WB
  • Homo sapiens (Human)
EBV-miR-BART22 induces β-catenin abnormally activated in the NPC cell lines.A Pathway based on the KEGG and TargetScan databases. B Pathway based on the KEGG and DIANA databases. C The nuclear fraction of indicated cells was analyzed by WB analysis. D–F Cells were treated with β-catenin siRNA and... more
EBV-miR-BART22 induces β-catenin abnormally activated in the NPC cell lines.A Pathway based on the KEGG and TargetScan databases. B Pathway based on the KEGG and DIANA databases. C The nuclear fraction of indicated cells was analyzed by WB analysis. D–F Cells were treated with β-catenin siRNA and plasmid β-catenin for 72 h, and then performed wound-healing assays and Transwell/migration assay. *P < 0.05. **P < 0.01. G Expression of epithelial cell marker, mesenchymal cell marker, and β-catenin in indicated cells were examined by WB analysis. GAPDH was used as a loading control. less

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Epstein-Barr virus-encoded microRNA BART22 serves as novel biomarkers and drives malignant transformation of nasopharyngeal carcinoma.

In Cell Death Dis on 30 July 2022 by Zhang, T., Chen, Z., et al.

Fig.7.J
Fig.7.J showing Western Blotting in a Homo sapiens (Human) sample from the publication: Epstein-Barr virus-encoded microRNA BART22 serves as novel biomarkers and drives malignant transformation of nasopharyngeal carcinoma.
  • WB
  • Homo sapiens (Human)
MOSPD2 is a direct target of EBV-miR-BART22.A A Venn diagram depicting the overlap of target genes predicted by TargetScan (green), RNA-sequencing (red), DIANA (blue), and Vir-Mir (yellow). Putative target genes identified by this approach are listed. B Quantitative reverse transcription-polymera... more
MOSPD2 is a direct target of EBV-miR-BART22.A A Venn diagram depicting the overlap of target genes predicted by TargetScan (green), RNA-sequencing (red), DIANA (blue), and Vir-Mir (yellow). Putative target genes identified by this approach are listed. B Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis of EBV-miR-BART22 regulation on target genes in nasopharyngeal carcinoma cells. C Expression of MOSPD2 in indicated cells was examined by WB analysis. D The relative expression levels of MOSPD2 in normal nasopharyngeal tissues and nasopharyngeal tumors in the GEO data set for nasopharyngeal carcinoma. E The construction of luciferase reporter vectors with inserted WT or mutant MOSPD2 3′-UTR sequences. F Changes in the normalized reporter gene activities of WT and mutant MOSPD2 3′-UTR luciferase reporter constructs responded to the co-transfection of negative control (NC) or EBV-miR-BART22 mimic in T293 cells. G Representative photomicrographs of scratch wounds at 0 and 24 h after wounds were made. Quantitative measurement of wound gaps by Photoshop software. H Quantification of indicated migrating cells in 5 random fields analyzed by Transwell assays, respectively. I Quantification of indicated migrating cells in 5 random fields analyzed by invasion assays, respectively. J Expression of epithelial cell marker, mesenchymal cell marker, β-catenin, and MOSPD2 in indicated cells were examined by WB analysis. GAPDH was used as a loading control. less

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PGC1α Cooperates with FOXA1 to Regulate Epithelial Mesenchymal Transition through the TCF4-TWIST1.

In Int J Mol Sci on 26 July 2022 by Fang, X. Q., Lee, M., et al.

Fig.3.B
Fig.3.B showing Western Blotting in a Homo sapiens (Human) sample from the publication: PGC1α Cooperates with FOXA1 to Regulate Epithelial Mesenchymal Transition through the TCF4-TWIST1.
  • WB
  • Homo sapiens (Human)
PGC1α and FOXA1 suppress EMT-associated gene expression. (A) EMT−related genes and (B) proteins expression in FOXA1 silenced A549 cells. (C) EMT gene expression in FOXA1 silenced H358 cells. (D) Alteration of EMT genes by ectopic GFP or FOXA1 expression upon TGFβ1. A549 cells were infected with a... more
PGC1α and FOXA1 suppress EMT-associated gene expression. (A) EMT−related genes and (B) proteins expression in FOXA1 silenced A549 cells. (C) EMT gene expression in FOXA1 silenced H358 cells. (D) Alteration of EMT genes by ectopic GFP or FOXA1 expression upon TGFβ1. A549 cells were infected with adenovirus (1000 pfu/cell) expressing GFP or FOXA1 and incubated for 48 h. After adenoviral transduction, cells were incubated with TGFβ1 (20 ng/mL) for 24 h. (E) EMT-associated genes expression in PGC1α silenced A549 cells upon TGFβ1 (20 ng/mL for 24 h). Upper (CDH1 and CDH2) and bottom (SNAI1 and SNAI2). (F) EMT-associated proteins expression in PGC1α silenced A549 cells upon TGFβ1 (20 ng/mL). Quantitative E−cadherin levels represented (right panel). (G) Changes of EMT−related gene in ectopic PGC1α expression upon TGFβ1. A549 cells were infected with PGC1α expressing lentivirus (1000 pfu/cell) and incubated for 48 h. After lentiviral transduction, cells were incubated with TGFβ1 (20 ng/mL) for 24 h. Values represent mean ± SD (n = 3). * p < 0.05, ** p < 0.01, and *** p < 0.001 by one-way ANOVA with Tukey post-test for multiple comparisons. less

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PGC1α Cooperates with FOXA1 to Regulate Epithelial Mesenchymal Transition through the TCF4-TWIST1.

In Int J Mol Sci on 26 July 2022 by Fang, X. Q., Lee, M., et al.

Fig.3.F
Fig.3.F showing Western Blotting in a Homo sapiens (Human) sample from the publication: PGC1α Cooperates with FOXA1 to Regulate Epithelial Mesenchymal Transition through the TCF4-TWIST1.
  • WB
  • Homo sapiens (Human)
PGC1α and FOXA1 suppress EMT-associated gene expression. (A) EMT−related genes and (B) proteins expression in FOXA1 silenced A549 cells. (C) EMT gene expression in FOXA1 silenced H358 cells. (D) Alteration of EMT genes by ectopic GFP or FOXA1 expression upon TGFβ1. A549 cells were infected with a... more
PGC1α and FOXA1 suppress EMT-associated gene expression. (A) EMT−related genes and (B) proteins expression in FOXA1 silenced A549 cells. (C) EMT gene expression in FOXA1 silenced H358 cells. (D) Alteration of EMT genes by ectopic GFP or FOXA1 expression upon TGFβ1. A549 cells were infected with adenovirus (1000 pfu/cell) expressing GFP or FOXA1 and incubated for 48 h. After adenoviral transduction, cells were incubated with TGFβ1 (20 ng/mL) for 24 h. (E) EMT-associated genes expression in PGC1α silenced A549 cells upon TGFβ1 (20 ng/mL for 24 h). Upper (CDH1 and CDH2) and bottom (SNAI1 and SNAI2). (F) EMT-associated proteins expression in PGC1α silenced A549 cells upon TGFβ1 (20 ng/mL). Quantitative E−cadherin levels represented (right panel). (G) Changes of EMT−related gene in ectopic PGC1α expression upon TGFβ1. A549 cells were infected with PGC1α expressing lentivirus (1000 pfu/cell) and incubated for 48 h. After lentiviral transduction, cells were incubated with TGFβ1 (20 ng/mL) for 24 h. Values represent mean ± SD (n = 3). * p < 0.05, ** p < 0.01, and *** p < 0.001 by one-way ANOVA with Tukey post-test for multiple comparisons. less

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PGC1α Cooperates with FOXA1 to Regulate Epithelial Mesenchymal Transition through the TCF4-TWIST1.

In Int J Mol Sci on 26 July 2022 by Fang, X. Q., Lee, M., et al.

Fig.5.B
Fig.5.B showing Western Blotting in a Homo sapiens (Human) sample from the publication: PGC1α Cooperates with FOXA1 to Regulate Epithelial Mesenchymal Transition through the TCF4-TWIST1.
  • WB
  • Homo sapiens (Human)
TGFβ1 decreases ID1 by suppressing FOXA1 and PGC1α. (A) PGC1α mRNA upon TGFβ1 (20 ng/mL) in a time−dependent manner. PGC1α mRNA levels in TGFβ1−treated cells were compared to BSA−treated cells at indicated time points (12 h, 24 h or 48 h), respectively. (B) PGC1α protein expression upon TGFβ1 (20... more
TGFβ1 decreases ID1 by suppressing FOXA1 and PGC1α. (A) PGC1α mRNA upon TGFβ1 (20 ng/mL) in a time−dependent manner. PGC1α mRNA levels in TGFβ1−treated cells were compared to BSA−treated cells at indicated time points (12 h, 24 h or 48 h), respectively. (B) PGC1α protein expression upon TGFβ1 (20 ng/mL) in a time-dependent manner. (C) FOXA1 mRNA in the absence or presence of TGFβ1 (20 ng/mL for 24 h). (D) ID1 and ID2 mRNA expression upon TGFβ1 (20 ng/mL) in a time-dependent manner. ID1 and ID2 mRNA levels in TGFβ1−treated cells were compared to BSA−treated cells at indicated time points (12 h, 24 h, or 48 h), respectively. (E) ID1 protein in TGFβ1−treated A549 and H358 cells in a time−dependent manner. Quantitative ID1 protein level represented (right panel). (F) Changes of ID1 and ID2 mRNA levels by TGFβ1 (20 ng/mL for 24 h) in ectopic FOXA1 or (G) PGC1α expressing A549 cells. Values represent mean ± SD (n = 3). * p < 0.05, ** p < 0.01, and *** p < 0.001 by unpaired Student’s t−test for two experimental comparisons and one-way ANOVA with Tukey post-test for multiple comparisons. less

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Downregulated ADAMTS1 Incorporating A2M Contributes to Tumorigenesis and Alters Tumor Immune Microenvironment in Lung Adenocarcinoma.

In Biology (Basel) on 16 May 2022 by Lee, H. C., Chang, C. Y., et al.

Fig.7.C
Fig.7.C showing Western Blotting from the publication: Downregulated ADAMTS1 Incorporating A2M Contributes to Tumorigenesis and Alters Tumor Immune Microenvironment in Lung Adenocarcinoma.
  • WB
Functional analysis of ADAMTS1 in lung adenocarcinoma. (A) The knockdown efficacy of shRNA transfection. (B) Cell migration of ADAMTS1 knockdown A549 cells, as determined by wound-healing. (C) EMT markers in the ADAMTS1 knockdown A549 cells. The uncropped western blot figures were presented in Fi... more
Functional analysis of ADAMTS1 in lung adenocarcinoma. (A) The knockdown efficacy of shRNA transfection. (B) Cell migration of ADAMTS1 knockdown A549 cells, as determined by wound-healing. (C) EMT markers in the ADAMTS1 knockdown A549 cells. The uncropped western blot figures were presented in Figure S1. (D) Tumor metastasis in mice lung after injection of control plasmid transfected and ADAMTS1-knockdown A549 cells. A549 cells were transfected with a control vector or ADAMTS1 shRNA plasmid and selected by puromycin. The cells were implanted into nude mice by tail vein injection, and the tumor nodules were counted after 21 days of inoculation. The data showed represent the mean ± SD (* p < 0.05, ** p < 0.01, **** p < 0.001). ns, not significant. less

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Upregulation of PEDF Predicts a Poor Prognosis and Promotes Esophageal Squamous Cell Carcinoma Progression by Modulating the MAPK/ERK Signaling Pathway.

In Front Oncol on 16 March 2021 by Chen, Z., Che, D., et al.

Fig.4.B
Fig.4.B showing Western Blotting from the publication: Upregulation of PEDF Predicts a Poor Prognosis and Promotes Esophageal Squamous Cell Carcinoma Progression by Modulating the MAPK/ERK Signaling Pathway.
  • WB
PEDF promotes ESCC cell migration, invasion, and EMT. (A) The KYSE510 and KYSE140 cellular migration and invasion capability were assessed by transwell migration and Boyden chamber invasion assays. The mean numbers of migrating or invading cells in the field were calculated by mean ± SD from thre... more
PEDF promotes ESCC cell migration, invasion, and EMT. (A) The KYSE510 and KYSE140 cellular migration and invasion capability were assessed by transwell migration and Boyden chamber invasion assays. The mean numbers of migrating or invading cells in the field were calculated by mean ± SD from three-time different experiments. Magnification for ×100. *P < 0.05, **P < 0.01, ***P < 0.001. (B) KYSE510 and KYSE140 cells and appropriate controls were used in a wound-healing assay. Scale bar = 100 μm. (n = 3 each). Data are means ± S.E.M. *P < 0.05, **P < 0.01. (C) The expression of α-catenin, N-cadherin, and E-cadherin were probed by western blotting in overexpress of PEDF KYSE510 and KYSE140 cells, and PEDF inhibition KYSE510 and KYSE140 cells, and the corresponding control cells. less

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Upregulation of PEDF Predicts a Poor Prognosis and Promotes Esophageal Squamous Cell Carcinoma Progression by Modulating the MAPK/ERK Signaling Pathway.

In Front Oncol on 16 March 2021 by Chen, Z., Che, D., et al.

Fig.5.B
Fig.5.B showing Western Blotting from the publication: Upregulation of PEDF Predicts a Poor Prognosis and Promotes Esophageal Squamous Cell Carcinoma Progression by Modulating the MAPK/ERK Signaling Pathway.
  • WB
MAPK/ERK signaling pathway is required for PEDF mediated EMT. (A) The expressions of AKT, p-AKT, a-catenin, ERK1/2, p-ERK1/2 and PEDF were probed by western blotting in the overexpression of PEDF KYSE510 and KYSE140 cells, and PEDF knockdown KYSE510 and KYSE140 cells, and the corresponding contro... more
MAPK/ERK signaling pathway is required for PEDF mediated EMT. (A) The expressions of AKT, p-AKT, a-catenin, ERK1/2, p-ERK1/2 and PEDF were probed by western blotting in the overexpression of PEDF KYSE510 and KYSE140 cells, and PEDF knockdown KYSE510 and KYSE140 cells, and the corresponding control cells. GAPDH was a protein loading control. (B) Western blotting indicated that p-ERK1/2 inhibitor PD98059 and U0126 inhibited PEDF induced the activation of MAPK/ERK signaling pathway, as well as the EMT-related characterizations in KYSE510 and KYSE140 cells. Cells were treated with MAPK/ERK signaling agonist PD98059 or U0126 for 24 h, and then performed WB assay. P < 0.05, relative to PD98059 or U0126 treatment of the same cell type as controls. (C) The cell invasion and migration were evaluated after ERK1/2 inhibitor treatment for 24 h. Magnification for × 100. *P < 0.05, **P < 0.01, ***P < 0.001. less

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Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy.

In Cells on 4 March 2021 by Seok, J. K., Hong, E. H., et al.

Fig.1.F
Fig.1.F showing Western Blotting from the publication: Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy.
  • WB
1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) induces changes in epithelial-mesenchymal transition marker expression in cancer cells. (A,B) HepG2 cells were treated with (A) the specified doses of POVPC for 48 h and (B) 5 µg/mL of POVPC for the indicated periods. The levels of... more
1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) induces changes in epithelial-mesenchymal transition marker expression in cancer cells. (A,B) HepG2 cells were treated with (A) the specified doses of POVPC for 48 h and (B) 5 µg/mL of POVPC for the indicated periods. The levels of EMT-related protein markers were determined by immunoblotting with β-actin as the loading control. (C) HepG2 cells were treated with 5 µg/mL of POVPC for 48 h. Expression of E-cadherin (green), N-cadherin (red), and vimentin (green) was determined using confocal immunofluorescence microscopy. Cells were identified by DAPI staining of the nuclei (blue). The scale bar represents 100 μm. (D) HepG2 cells were treated with 5 µg/mL of POVPC for the indicated periods. The levels of transcription factors (Snail, Slug, and Twist) were determined by immunoblotting with β-actin as the loading control. (E,F) MCF7 cells were treated with (E) the specified doses of POVPC for 48 h and (F) 5 µg/mL of POVPC for the indicated periods. The protein levels of EMT-related markers were determined by immunoblotting with β-actin as the loading control. (G) MCF7 cells were treated with 5 µg/mL of POVPC for 48 h and processed as described in C. (H) MCF7 cells were treated with 5 µg/mL of POVPC for the indicated periods and processed as described in (D). less

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Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy.

In Cells on 4 March 2021 by Seok, J. K., Hong, E. H., et al.

Fig.1.A
Fig.1.A showing Western Blotting from the publication: Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy.
  • WB
1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) induces changes in epithelial-mesenchymal transition marker expression in cancer cells. (A,B) HepG2 cells were treated with (A) the specified doses of POVPC for 48 h and (B) 5 µg/mL of POVPC for the indicated periods. The levels of... more
1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) induces changes in epithelial-mesenchymal transition marker expression in cancer cells. (A,B) HepG2 cells were treated with (A) the specified doses of POVPC for 48 h and (B) 5 µg/mL of POVPC for the indicated periods. The levels of EMT-related protein markers were determined by immunoblotting with β-actin as the loading control. (C) HepG2 cells were treated with 5 µg/mL of POVPC for 48 h. Expression of E-cadherin (green), N-cadherin (red), and vimentin (green) was determined using confocal immunofluorescence microscopy. Cells were identified by DAPI staining of the nuclei (blue). The scale bar represents 100 μm. (D) HepG2 cells were treated with 5 µg/mL of POVPC for the indicated periods. The levels of transcription factors (Snail, Slug, and Twist) were determined by immunoblotting with β-actin as the loading control. (E,F) MCF7 cells were treated with (E) the specified doses of POVPC for 48 h and (F) 5 µg/mL of POVPC for the indicated periods. The protein levels of EMT-related markers were determined by immunoblotting with β-actin as the loading control. (G) MCF7 cells were treated with 5 µg/mL of POVPC for 48 h and processed as described in C. (H) MCF7 cells were treated with 5 µg/mL of POVPC for the indicated periods and processed as described in (D). less

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Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy.

In Cells on 4 March 2021 by Seok, J. K., Hong, E. H., et al.

Fig.1.B
Fig.1.B showing Western Blotting from the publication: Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy.
  • WB
1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) induces changes in epithelial-mesenchymal transition marker expression in cancer cells. (A,B) HepG2 cells were treated with (A) the specified doses of POVPC for 48 h and (B) 5 µg/mL of POVPC for the indicated periods. The levels of... more
1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) induces changes in epithelial-mesenchymal transition marker expression in cancer cells. (A,B) HepG2 cells were treated with (A) the specified doses of POVPC for 48 h and (B) 5 µg/mL of POVPC for the indicated periods. The levels of EMT-related protein markers were determined by immunoblotting with β-actin as the loading control. (C) HepG2 cells were treated with 5 µg/mL of POVPC for 48 h. Expression of E-cadherin (green), N-cadherin (red), and vimentin (green) was determined using confocal immunofluorescence microscopy. Cells were identified by DAPI staining of the nuclei (blue). The scale bar represents 100 μm. (D) HepG2 cells were treated with 5 µg/mL of POVPC for the indicated periods. The levels of transcription factors (Snail, Slug, and Twist) were determined by immunoblotting with β-actin as the loading control. (E,F) MCF7 cells were treated with (E) the specified doses of POVPC for 48 h and (F) 5 µg/mL of POVPC for the indicated periods. The protein levels of EMT-related markers were determined by immunoblotting with β-actin as the loading control. (G) MCF7 cells were treated with 5 µg/mL of POVPC for 48 h and processed as described in C. (H) MCF7 cells were treated with 5 µg/mL of POVPC for the indicated periods and processed as described in (D). less

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Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy.

In Cells on 4 March 2021 by Seok, J. K., Hong, E. H., et al.

Fig.1.E
Fig.1.E showing Western Blotting from the publication: Oxidized Phospholipids in Tumor Microenvironment Stimulate Tumor Metastasis via Regulation of Autophagy.
  • WB
1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) induces changes in epithelial-mesenchymal transition marker expression in cancer cells. (A,B) HepG2 cells were treated with (A) the specified doses of POVPC for 48 h and (B) 5 µg/mL of POVPC for the indicated periods. The levels of... more
1-palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC) induces changes in epithelial-mesenchymal transition marker expression in cancer cells. (A,B) HepG2 cells were treated with (A) the specified doses of POVPC for 48 h and (B) 5 µg/mL of POVPC for the indicated periods. The levels of EMT-related protein markers were determined by immunoblotting with β-actin as the loading control. (C) HepG2 cells were treated with 5 µg/mL of POVPC for 48 h. Expression of E-cadherin (green), N-cadherin (red), and vimentin (green) was determined using confocal immunofluorescence microscopy. Cells were identified by DAPI staining of the nuclei (blue). The scale bar represents 100 μm. (D) HepG2 cells were treated with 5 µg/mL of POVPC for the indicated periods. The levels of transcription factors (Snail, Slug, and Twist) were determined by immunoblotting with β-actin as the loading control. (E,F) MCF7 cells were treated with (E) the specified doses of POVPC for 48 h and (F) 5 µg/mL of POVPC for the indicated periods. The protein levels of EMT-related markers were determined by immunoblotting with β-actin as the loading control. (G) MCF7 cells were treated with 5 µg/mL of POVPC for 48 h and processed as described in C. (H) MCF7 cells were treated with 5 µg/mL of POVPC for the indicated periods and processed as described in (D). less

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Targeting endothelin 1 receptor-miR-200b/c-ZEB1 circuitry blunts metastatic progression in ovarian cancer.

In Commun Biol on 13 November 2020 by Sestito, R., Cianfrocca, R., et al.

Fig.1.A
Fig.1.A showing Western Blotting from the publication: Targeting endothelin 1 receptor-miR-200b/c-ZEB1 circuitry blunts metastatic progression in ovarian cancer.
  • WB
The expression of ETAR/ZEB1 is upregulated in ovarian cancers and correlates with poor prognosis.a Expression of ETAR, ZEB1, N-cadherin, Vimentin, and E-cadherin in ovarian cancer cell lines analyzed by Western blotting (WB). β-actin is used as loading control. b Correlation of the ETAR and ZEB1 ... more
The expression of ETAR/ZEB1 is upregulated in ovarian cancers and correlates with poor prognosis.a Expression of ETAR, ZEB1, N-cadherin, Vimentin, and E-cadherin in ovarian cancer cell lines analyzed by Western blotting (WB). β-actin is used as loading control. b Correlation of the ETAR and ZEB1 expression in the indicated cell lines. The ratio of ETAR/β-actin and ZEB1/β-actin, evaluated by WB as shown in a, is presented as bar and line, respectively. Values are the mean ± SD (n = 3). c Boxplot diagrams of EDNRA (ETAR) and ZEB1 gene expression in HG-SOC patients from TCGA, subdivided in four molecular subtypes. d Kaplan–Meier curves of overall survival (OS) of 352 patients from TCGA grouped in high EDNRA/ZEB1 levels (160 patients, z-score > 1.5, red line) and low EDNRA/ZEB1 expression levels (192 patients, z-score < 1.5, blue line). e Kaplan–Meier curves of progression-free survival (PFS) of 303 patients from TCGA subdivided in high levels of EDNRA/ZEB1 expression (135 patients, z-score > 1.5, red line) and low levels of EDNRA/ZEB1 (168 patients, z-score < 1.5, blue line). less

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Targeting endothelin 1 receptor-miR-200b/c-ZEB1 circuitry blunts metastatic progression in ovarian cancer.

In Commun Biol on 13 November 2020 by Sestito, R., Cianfrocca, R., et al.

Fig.6.B
Fig.6.B showing Western Blotting from the publication: Targeting endothelin 1 receptor-miR-200b/c-ZEB1 circuitry blunts metastatic progression in ovarian cancer.
  • WB
The integrated circuit ETAR-miR-200b/c-ZEB1 is involved in ET-1-dependent protease activation, EMT, cell plasticity, and invasion.a Conditioned media from SKOV3 cells transfected with siRNA control (si-Ctr), si-ZEB1, or mimic-miR-200b/c (miR-200b/c), or treated with MAC, stimulated or not with ET... more
The integrated circuit ETAR-miR-200b/c-ZEB1 is involved in ET-1-dependent protease activation, EMT, cell plasticity, and invasion.a Conditioned media from SKOV3 cells transfected with siRNA control (si-Ctr), si-ZEB1, or mimic-miR-200b/c (miR-200b/c), or treated with MAC, stimulated or not with ET-1 for 48 h are analyzed by gelatin zymography to detect the active forms of MMP-2/9. b Expression of E-cadherin, N-cadherin, Vimentin, and ZEB1 proteins is analyzed by WB in SKOV3 cells transfected and stimulated as in a. β-actin is used as loading control. c E-cadherin, ZEB1, N-cadherin, and Vimentin gene expression in SKOV3 cells transfected with si-Ctr, si-ZEB1, si-ETAR, or mimic-miR-200b/c (miR-200b/c), and treated as in b is analyzed by qRT-PCR and normalized to cyclophilin-A. Values are the mean ± SD (n = 3; *p < 0.02 vs. si-Ctr; **p < 0.004 vs. ET-1 stimulated si-Ctr). d Luciferase activity in SKOV3 cells transfected as in c and co-transfected with the E-cadherin promoter reporter plasmid and stimulated with ET-1 and/or MAC for 48 h. Values are the mean ± SD expressed as fold induction (n = 3; *p < 0.002 vs. si-Ctr; **p < 0.004 vs. ET-1 stimulated si-Ctr). e Assay of tubule-like structure formation in SKOV3 cells transfected for 48 h as in c and overnight stimulated or not with ET-1. Original magnification 20×. (Scale bar: 100 μm). Graphs represent the quantification of the number of nodes and the tube length. Columns show the mean ± SD (n = 3; *p < 0.02 vs. unstimulated Ctr; **p < 0.001 vs. ET-1-stimulated Ctr). f Chemoinvasion assay in SKOV3 cells transfected as in c and overnight stimulated or not with ET-1. Images represent the crystal violet-stained invasive cells. Magnification ×10. Graph represents the number of invading cells. Columns show the mean ± SD (n = 3; *p < 0.001 vs. unstimulated Ctr; **p < 0.001 vs. ET-1-stimulated Ctr). less

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Targeting the TGFβ pathway in uterine carcinosarcoma.

In Cell Stress on 25 August 2020 by Dwivedi, S. K. D., Rao, G., et al.

Fig.3.B
Fig.3.B showing Western Blotting from the publication: Targeting the TGFβ pathway in uterine carcinosarcoma.
  • WB
FIGURE 3: GLT inhibits canonical and non-canonical TGFβ signaling.CS-99 and UMMT-ARK1 cells were grown on a thin layer of Matrigel and treated with TGFβ1, GLT and Cisplatin (CIS, 2.5 µM) as represented, post 24 h of treatment, cell lysate was immunoblotted for (A) canonical and non-canonical mark... more
FIGURE 3: GLT inhibits canonical and non-canonical TGFβ signaling.CS-99 and UMMT-ARK1 cells were grown on a thin layer of Matrigel and treated with TGFβ1, GLT and Cisplatin (CIS, 2.5 µM) as represented, post 24 h of treatment, cell lysate was immunoblotted for (A) canonical and non-canonical markers of TGFβ1 signaling proteins along with Cyclin D1 as a marker for cell cycle progression and Tubulin as the loading control. (B) Effect of TGFβ1 and GLT + TGFβ1 treatment on the EMT markers (FBN – Fibronectin, NCAD - N-cadherin) were evaluated using immunoblotting, GAPDH was used as the loading control. less

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Targeting the TGFβ pathway in uterine carcinosarcoma.

In Cell Stress on 25 August 2020 by Dwivedi, S. K. D., Rao, G., et al.

Fig.4.E
Fig.4.E showing Western Blotting from the publication: Targeting the TGFβ pathway in uterine carcinosarcoma.
  • WB
FIGURE 4: GLT sensitizes tumor cells to chemotherapy in a mouse model.(A) Female athymic nude mice were subcutaneously injected with CS-99 cells, once the tumor reached to ~100 mm3, tumor bearing mice were randomized into four groups (n = 7-10) and treated with either control vehicle (V), GLT, ca... more
FIGURE 4: GLT sensitizes tumor cells to chemotherapy in a mouse model.(A) Female athymic nude mice were subcutaneously injected with CS-99 cells, once the tumor reached to ~100 mm3, tumor bearing mice were randomized into four groups (n = 7-10) and treated with either control vehicle (V), GLT, carboplatin & paclitaxel (CT), or GLT + CT. Treatment continued for two cycles (14 days), and mice were followed for survival. (B) Relative tumor volume normalized with V (vehicle) group. (C) Tumor doubling time (TDT) was calculated for each treatment groups according to Mehrara and colleagues [35]. Data are mean ± SD and *, P < 0.05 when comparing between indicated groups by one-way ANOVA (D) Percent survival was calculated by Kaplan–Meier method and P values determined by log-rank test based on the number of days the animals survived before the euthanization as per IACUC limits (humane endpoint). (E) Four tumor samples from vehicle treated control and GLT treated group were analyzed for the expression of TGFβ1 signaling and EMT markers using immunoblotting, alpha tubulin was used as loading control. Values are mean ±SD. *P<0.05. less

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