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Caveolin-2 is regulated by BRD4 and contributes to cell growth in pancreatic cancer

Feng Jiao1, Ting Han1, Cuncun Yuan2

  • 11Department of Oncology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, 160 Pujian Road, Shanghai, 200127 China.

Cancer Cell International
|February 27, 2020
PubMed
Abstract

Insights

Bromodomain and extra-terminal domain (BET) protein BRD4 promotes pancreatic cancer growth and progression by upregulating caveolin-2. Targeting this interaction offers a potential therapeutic strategy for pancreatic cancer.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Bromodomain and extra-terminal domain (BET) proteins, particularly BRD4, are crucial for epigenetic regulation and cell survival.
  • BRD4 is a promising target for anticancer therapies.
  • Pancreatic cancer progression involves complex molecular mechanisms that require further elucidation.

Purpose of the Study:

  • To investigate the role of BRD4 in pancreatic cancer cell growth and progression.
  • To identify novel mechanisms underlying BRD4's function in pancreatic cancer.
  • To explore the potential of targeting BRD4 as a therapeutic strategy.

Main Methods:

  • Western blotting, immunohistochemistry, and real-time PCR were used to analyze BRD4 expression in patient tissues.
  • In vitro assays (colony formation, sulforhodamine B, Transwell) and in vivo studies in nude mice assessed BRD4's effects on cell proliferation, migration, and invasion.
  • RNA sequencing, ChIP, and dual luciferase reporter assays identified downstream targets and molecular mechanisms.

Main Results:

  • BRD4 was overexpressed in pancreatic cancer and promoted cell proliferation, migration, and invasion in vitro and in vivo.
  • Caveolin-2 was identified as a downstream target of BRD4, with BRD4 binding to its promoter region and upregulating its expression.
  • High expression of both BRD4 and caveolin-2 correlated with shorter patient survival, and both were identified as independent prognostic factors.

Conclusions:

  • BRD4 exhibits oncogenic effects in pancreatic cancer, partly through the upregulation of caveolin-2, enhancing cell growth.
  • The BRD4-caveolin-2 interaction represents a potential therapeutic target for pancreatic cancer.
  • Development of BET inhibitors targeting the BRD4-caveolin-2 interaction could be a viable treatment strategy.
Keywords:
BET inhibitorsBRD4Caveolin-2Pancreatic cancer

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