ArticleCancer cell international2020
Caveolin-2 is regulated by BRD4 and contributes to cell growth in pancreatic cancer.
Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Identification of prognostic lipid droplet-associated genes in pancreatic cancer patients via bioinformatics analysis.Lipids in health and disease · 2021Pooled it
- Disrupting lipid homeostasis with CAV2 in OSCC triggers apoptosis, lipolysis, and mitochondrial dysfunction by transcriptional repression of PPARγ.Cell & bioscience · 2025Article
- Caveolin 1 and 2 enhance the proliferative capacity of BCAM-positive corneal progenitors.Scientific reports · 2025Article
- Location and Movement of the Oxytocin Receptor Differ Between the Normal and Diseased Prostate.Cancers · 2025Article
- ATG10S promotes IFNL1 expression and autophagic degradation of multiple viral proteins mediated by IFNL1.Autophagy · 2024Article
- Identification and validation of eight lysosomes-related genes signatures and correlation with immune cell infiltration in lung adenocarcinoma.Cancer cell international · 2023Article
- Transcriptional co-activators: emerging roles in signaling pathways and potential therapeutic targets for diseases.Signal transduction and targeted therapy · 2023Review
- The RGG motif proteins: Interactions, functions, and regulations.Wiley interdisciplinary reviews. RNA · 2023Review
- PROTACs in gastrointestinal cancers.Molecular therapy oncolytics · 2022Review
- Disease-related protein co-expression networks are associated with the prognosis of resectable node-positive pancreatic ductal adenocarcinoma.Scientific reports · 2022Article
- Identification and validation of a seven-gene prognostic marker in colon cancer based on single-cell transcriptome analysis.IET systems biology · 2022Article
- Bromodomain and extra-terminal inhibitors emerge as potential therapeutic avenues for gastrointestinal cancers.World journal of gastrointestinal oncology · 2022Review
- CAV2 Regulates Mir-4723/Wnt7A Signalling Axis through Endocytosis and Epithelial-Mesenchymal Transition to Promote Proliferation, Invasion, and Metastasis of Pancreatic Cancer Cells.Journal of Cancer · 2022Article
- Caveolae and Lipid Rafts in Endothelium: Valuable Organelles for Multiple Functions.Biomolecules · 2020Review
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7 authors.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe bromodomain and extra-terminal domain (BET) family of proteins, especially BRD4 play an important role in epigenetic regulation, and are essential for cell survival and also are promising anticancer targets. This study aims to analyze the effect of BRD4 on the cell growth and progression of pancreatic cancer and novel mechanisms involved.
methodsExpression of BRD4 in pancreatic cancer and paired adjacent noncancerous tissues from 76 patients was analyzed by western blotting, immunohistochemistry, and real time PCR. Its correlation with the clinicopathological characteristics and prognosis of pancreatic cancer patients was analyzed. The effects of BRD4 on the cell proliferation were detected by colony formation assay and sulforhodamine B assay. Migration and invasion were determined by Transwell assays, and the effect of BRD4 on subcutaneous tumor formation was verified in nude mice. Cell cycle analysis was detected by flow cytometry. The potential downstream targets of BRD4 and related molecular mechanisms were clarified by RNA sequencing, chromatin immunoprecipitation and dual luciferase reporter assay.
resultsBRD4 was overexpressed in pancreatic cancer. Biological results showed that BRD4 functioned as tumor promoter, facilitated cell proliferation, migration and invasion in vitro and in vivo. Further, caveolin-2 was selected as the downstream gene of BRD4 by RNA sequencing. Caveolin-2 overexpression can partially reverse the decreased cell growth ability caused by BRD4 knockdown, but did not affect cell migration and invasion. Chromatin immunoprecipitation assay and dual luciferase reporter assay revealed BRD4 could bind to the promoter region of caveolin-2 and upregulate caveolin-2 expression. Clinical data further indicated a positive correlation between BRD4 and caveolin-2 expression. BRD4 (high)/caveolin-2 (high) correlated with shorter overall survival of patients with pancreatic cancer. Multivariate analysis revealed that both BRD4 and caveolin-2 were independent factors.
conclusionsOur findings reveal the oncogenic effects of BRD4 in pancreatic cancer and elucidate a possible mechanism by which BRD4 and caveolin-2 act to enhance cell growth. Targeting the BRD4-caveolin-2 interaction by development of BET inhibitors will be a therapeutic strategy for pancreatic cancer.
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