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Updated: May 10, 2026

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells
09:24

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Published on: August 12, 2015

BRCA1 expression is epigenetically repressed in sporadic ovarian cancer cells by overexpression of C-terminal binding

Taymaa May1, Junzheng Yang, Melina Shoni

  • 1Department of Obstetrics/Gynecology and Reproductive Biology, Division of Gynecologic Oncology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

Neoplasia (New York, N.Y.)
|June 5, 2013
PubMed
Abstract

Insights

C-terminal binding protein 2 (CtBP2) is an oncogene in ovarian cancer that silences BRCA1. Inhibiting CtBP2 with MTOB may be an effective treatment for ovarian cancer patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Ovarian cancer remains a leading cause of gynecological cancer mortality.
  • C-terminal binding protein 2 (CtBP2) is overexpressed in epithelial ovarian carcinoma.

Purpose of the Study:

  • To investigate the role of CtBP2 in ovarian cancer pathogenesis.
  • To explore CtBP2's regulation of BRCA1.
  • To evaluate CtBP2 inhibitors as a potential therapeutic strategy.

Main Methods:

  • Gene expression analysis using microarrays.
  • Chromatin immunoprecipitation (ChIP) and luciferase assays.
  • Immunohistochemical analysis of ovarian tumor tissues.
  • Drug sensitivity assays with CtBP2 inhibitor MTOB and PARP inhibitor Olaparib.

Main Results:

  • CtBP2 differentially regulates 85 genes, including those in the BRCA1 network.
  • CtBP2 binds to and represses the BRCA1 promoter.
  • Inverse correlation between CtBP2 and BRCA1 expression in ovarian tumors.
  • CtBP2 inhibitor MTOB suppresses ovarian cancer cell survival.

Conclusions:

  • CtBP2 acts as an oncogene in ovarian cancer by epigenetically silencing BRCA1.
  • CtBP2-specific inhibitors like MTOB show promise as adjunct therapies for CtBP2-positive ovarian cancer.

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