Journal: Clinical Epigenetics

Article Title: DNA methylation-mediated silencing of HNF1B promotes bladder cancer progression

doi: 10.1186/s13148-026-02079-z

Figure Lengend Snippet: Association of HNF1B with prognosis and clinicopathological characteristics in BLCA. A Kaplan–Meier analysis of OS and PFS in the TCGA-BLCA cohort stratified by high vs. low HNF1B expression. B HNF1B expression levels across clinicopathological features and molecular subtypes (Urothelial-like [Uro], Genomically Unstable [GU], Basal/Squamous-like [Ba/Sq], Mesenchymal-like [Mes-like], Stem-like/Neuroendocrine-like [Sc/NE-like]) in the TCGA-BLCA cohort. C Validation of HNF1B expression associations with clinicopathological features (MIBC, muscle-invasive; NMIBC, non-muscle invasive) and molecular subtypes in the Xiangya cohort. D Mutational landscape of TCGA-BLCA tumors stratified by HNF1B expression (high vs. low). F. Forest plot from multivariable Cox regression analysis for OS in TCGA-BLCA cohort. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

Article Snippet: Lentiviral particles for HNF1B overexpression, knockdown (Table S3), and their respective negative controls (empty vector and scrambled shRNA) were purchased from GeneChem Co., Ltd. (Shanghai, China).

Techniques: Expressing, Biomarker Discovery

Journal: Clinical Epigenetics

Article Title: DNA methylation-mediated silencing of HNF1B promotes bladder cancer progression

doi: 10.1186/s13148-026-02079-z

Figure Lengend Snippet: HNF1B expression and its functional impact on BLCA cell proliferation. A HNF1B expression at mRNA and protein levels across five BLCA cell lines. B , C Validation of HNF1B knockdown (shHNF1B-1/2/3 vs. shCtrl) and overexpression (OE vs. Ctrl) efficiency by qRT-PCR ( B ) and Western blot ( C ). D Cell proliferation measured by CCK-8 assay following HNF1B knockdown or overexpression. E Clonogenic survival assessed by colony formation assay following HNF1B knockdown or overexpression. ns, not significant, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

Article Snippet: Lentiviral particles for HNF1B overexpression, knockdown (Table S3), and their respective negative controls (empty vector and scrambled shRNA) were purchased from GeneChem Co., Ltd. (Shanghai, China).

Techniques: Expressing, Functional Assay, Biomarker Discovery, Knockdown, Over Expression, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Colony Assay

Journal: Clinical Epigenetics

Article Title: DNA methylation-mediated silencing of HNF1B promotes bladder cancer progression

doi: 10.1186/s13148-026-02079-z

Figure Lengend Snippet: Regulatory role of HNF1B in BLCA cell migration and invasion. A Effects of HNF1B knockdown or overexpression on cell migration, assessed by wound healing assays. B Effects of HNF1B knockdown or overexpression on cell migration and invasion, assessed by Transwell assays. * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: Lentiviral particles for HNF1B overexpression, knockdown (Table S3), and their respective negative controls (empty vector and scrambled shRNA) were purchased from GeneChem Co., Ltd. (Shanghai, China).

Techniques: Migration, Knockdown, Over Expression

Journal: Clinical Epigenetics

Article Title: DNA methylation-mediated silencing of HNF1B promotes bladder cancer progression

doi: 10.1186/s13148-026-02079-z

Figure Lengend Snippet: In vivo tumor-suppressive effect of HNF1B in BLCA. A Macroscopic appearance of mice and xenograft tumors at endpoint (OE vs. Ctrl). B Xenograft growth kinetics (OE vs. Ctrl). C Comparison of final xenograft weights (OE vs. Ctrl). D Representative HE and IHC (HNF1B, Ki67) staining in tumor sections from the indicated groups. * P < 0.05, ** P < 0.01, **** P < 0.0001

Article Snippet: Lentiviral particles for HNF1B overexpression, knockdown (Table S3), and their respective negative controls (empty vector and scrambled shRNA) were purchased from GeneChem Co., Ltd. (Shanghai, China).

Techniques: In Vivo, Comparison, Staining

Journal: Clinical Epigenetics

Article Title: DNA methylation-mediated silencing of HNF1B promotes bladder cancer progression

doi: 10.1186/s13148-026-02079-z

Figure Lengend Snippet: Epigenetic regulation of HNF1B via promoter methylation in BLCA. A Correlation between DNA methylation across HNF1B gene region and its mRNA levels in TCGA-BLCA cohort. B Association between methylation at HNF1B promoter sites (cg12788467, cg13230606, cg19378036) and patient prognosis in TCGA-BLCA cohort. C HNF1B promoter methylation patterns in three BLCA cell lines assessed by BSP. D Reactivation of HNF1B expression 5-AzaC treatment in UM-UC-3 and 5637 cells. E Correlation between HNF1B promoter methylation and expression in an independent clinical cohort. F. Association between HNF1B promoter methylation and clinicopathological variables in the clinical cohort. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

Article Snippet: Lentiviral particles for HNF1B overexpression, knockdown (Table S3), and their respective negative controls (empty vector and scrambled shRNA) were purchased from GeneChem Co., Ltd. (Shanghai, China).

Techniques: Methylation, DNA Methylation Assay, Expressing

Journal: Clinical Epigenetics

Article Title: DNA methylation-mediated silencing of HNF1B promotes bladder cancer progression

doi: 10.1186/s13148-026-02079-z

Figure Lengend Snippet: Downstream signaling and validation of HNF1B in BLCA. A Hallmark gene set enrichment analysis of DEGs from HNF1B-knockdown T24 (shHNF1B-3 vs. shCtrl) and HNF1B-overexpressing 5637 (OE vs. Ctrl) cells. B Protein expression analysis of MAPK/EMT pathways in HNF1B-knockdown T24 (shHNF1B-3 vs. shCtrl) and HNF1B-overexpressing 5637 (OE vs. Ctrl) cells. C Representative images of multiplex immunofluorescence analysis of HNF1B and MAPK pathway activity in clinical BLCA samples. Chromatic assignments: blue (DAPI), green (pMEK1/2), red (pERK1/2), pink (HNF1B), orange (MEK1/2), purple (ERK1/2). D Correlation heatmap of HNF1B expression and MAPK pathway activity. E Comparison of MAPK pathway activity grouped by HNF1B expression. F , G Pharmacological rescue with trametinib in HNF1B-knockdown T24 ( F ) and HNF1B-overexpressing 5637 ( G ) cells. Statistical comparisons were performed within each cell line between the vehicle and trametinib-treated groups, with significance denoted by asterisks above the corresponding colored bars/lines. ns, not significant, * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: Lentiviral particles for HNF1B overexpression, knockdown (Table S3), and their respective negative controls (empty vector and scrambled shRNA) were purchased from GeneChem Co., Ltd. (Shanghai, China).

Techniques: Biomarker Discovery, Knockdown, Expressing, Multiplex Assay, Immunofluorescence, Activity Assay, Comparison

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Loss of Brg1 and Pten in Pancreatic Ductal Cells Forms Intraductal Tubulopapillary Neoplasm via the YAP/TAZ Pathway

doi: 10.1016/j.jcmgh.2025.101639

Figure Lengend Snippet: HPB mice exhibited increased proliferation and dedifferentiation of pancreatic ductal cells. ( A ) IHC detection of nuclear Ki-67 expression in the pancreatic sections from H, HB, HP, and HPB mice. Scale bar, 20 μm. ( B ) IHC detection of nuclear Pdx1, Sox9, and Hnf1β expression in the pancreatic sections from H, HB, HP, and HPB mice. Scale bar, 20 μm. ( C ) Quantification of Ki-67 by IHC. The Ki-67 positivity rate was significantly higher in HPB mice than in H , HB, and HP mice. Data are presented as the means ± SDs (n = 3 per group). P value was evaluated using a 1-way ANOVA with Dunnett’s post-hoc test. ( D ) Quantification of Pdx1, Sox9, and Hnf1β by IHC. The Pdx1 positivity rate was significantly higher in HPB mice than in H , HB, and HP mice, whereas the positivity rates for Sox9 and Hnf1β were significantly lower in HPB mice than in the H, HB, and HP mice. Data are presented as the means ± SDs (n = 3 per group). P value was evaluated using a 1-way ANOVA with Dunnett’s post-hoc test.

Article Snippet: HNF1β , Proteintech , 1:200 , 12533-1-AP.

Techniques: Expressing

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Loss of Brg1 and Pten in Pancreatic Ductal Cells Forms Intraductal Tubulopapillary Neoplasm via the YAP/TAZ Pathway

doi: 10.1016/j.jcmgh.2025.101639

Figure Lengend Snippet: Blocking of YAP/TAZ activation inhibits the dedifferentiation of pancreatic ductal cells and tumor formation in HPB mice. ( A ) Experimental scheme for the tamoxifen-induced genetic recombination and treatment protocol. HPB mice were treated with VP, an inhibitor of the connection of YAP/TAZ and TEAD or vehicle. ( B ) Representative images of H&E staining of the pancreas from HPB mice treated with VP or vehicle. At 28 days after the first tamoxifen injection, tumor formation in the pancreatic ductal cells was partially suppressed in HPB mice following VP administration. Scale bar, 20 μm. ( C ) Tumor formation in HPB mice treated with VP or vehicle. n = 5 per group. Scale bar, 20 μm. ( D ) IHC for Ki-67, Pdx1, Sox9 and Hnf1β in HPB mice treated with VP or vehicle. n = 3 per group. Scale bar, 20 μm. ( E ) Quantification of IHC staining for Ki-67, Pdx1, Sox9, and Hnf1β in HPB mice treated with VP or vehicle. The Ki-67 positivity rate was significantly higher in HPB mice treated with VP. The Pdx1 positivity rate was significantly reduced, whereas Sox9 and Hnf1β positivity rates were significantly elevated in HPB mice following VP administration. Data are presented as the means ± SDs (n = 3 per group). The P values were evaluated using a 2-tailed Student’s t -test. ( F ) IHC for Yap, Taz, Birc5, and Ctgf in HPB mice treated with VP or vehicle. n = 3 per group. Scale bar, 20 μm.

Article Snippet: HNF1β , Proteintech , 1:200 , 12533-1-AP.

Techniques: Blocking Assay, Activation Assay, Staining, Injection, Immunohistochemistry