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Aberrant epigenetic regulation of bromodomain BRD4 in human colon cancer

R M Rodriguez1, C Huidobro, R G Urdinguio

  • 1Cancer Epigenetics Laboratory, Instituto Universitario de Oncología del Principado de Asturias (IUOPA), HUCA, Universidad de Oviedo, Oviedo, Spain.

Journal of Molecular Medicine (Berlin, Germany)
|November 29, 2011
PubMed

Insights

Bromodomain protein BRD4, crucial for cell cycle, is downregulated in colon cancer due to promoter hypermethylation. Restoring BRD4 levels inhibited tumor growth, indicating its tumor-suppressive role.

Area of Science:

  • Molecular biology
  • Cancer research
  • Epigenetics

Background:

  • Bromodomain protein BRD4 regulates cell proliferation and cell cycle progression.
  • BRD4 functions in the epigenetic regulation of transcription at targeted loci.
  • Aberrant gene silencing through promoter hypermethylation is a hallmark of cancer.

Purpose of the Study:

  • To investigate the role of BRD4 in human colon cancer.
  • To determine if BRD4 is epigenetically silenced in colon cancer.
  • To assess the therapeutic potential of BRD4 re-expression in colon cancer models.

Main Methods:

  • Analysis of BRD4 expression in colon cancer cell lines and primary tumors.
  • Assessment of promoter methylation status of BRD4.
  • In vivo tumor growth assays following ectopic BRD4 re-expression.

Main Results:

  • BRD4 was found to be frequently downregulated in human colon cancer cell lines and primary tumors.
  • Downregulation of BRD4 correlated with aberrant promoter hypermethylation.
  • Ectopic re-expression of BRD4 significantly reduced in vivo tumor growth in colon cancer cell lines.

Conclusions:

  • BRD4 acts as a tumor suppressor in human colon cancer.
  • Epigenetic silencing of BRD4 via promoter hypermethylation contributes to colon cancer development.
  • BRD4 re-expression represents a potential therapeutic strategy for colon cancer.

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