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VDAC1 is regulated by BRD4 and contributes to JQ1 resistance in breast cancer

Guochao Yang1, Dianwei Zhou2, Jun Li3

  • 1Department of General Surgery, Rongjun Hospital, Wuhan, Hubei 430079, P.R. China.

Oncology Letters
|August 28, 2019
PubMed

Insights

Voltage-dependent anion channel 1 (VDAC1) promotes breast cancer growth and is linked to poor patient prognosis. BRD4 regulates VDAC1, which may contribute to therapeutic resistance in breast cancer.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Oncology

Background:

  • Voltage-dependent anion channels (VDACs) regulate mitochondrial transport.
  • VDAC1 is overexpressed in various cancers, but its role in breast cancer is unclear.

Purpose of the Study:

  • Investigate the biological role and regulatory mechanisms of VDAC1 in breast cancer.
  • Determine VDAC1's association with clinicopathological features and patient prognosis.

Main Methods:

  • MTS assay for cell proliferation.
  • Gene Expression Profiling Interactive Analysis for clinical associations.
  • Western blot, qPCR, ChIP, and ChIP-qPCR for regulatory analysis.

Main Results:

  • VDAC1 overexpression promotes breast cancer cell proliferation.
  • VDAC1 expression correlates with poor prognosis in breast cancer patients.
  • Bromodomain inhibitor JQ1 reduces VDAC1 expression; BRD4 regulates VDAC1.
  • VDAC1 may confer resistance to JQ1 in breast cancer.

Conclusions:

  • VDAC1 plays a significant role in breast cancer progression.
  • BRD4 is a key regulator of VDAC1 in breast cancer.
  • VDAC1 presents a potential therapeutic target for breast cancer treatment.
Keywords:
breast cancerbromodomain inhibitorsbromodomain-containing protein 4drug resistancevoltage-dependent anion channel 1

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