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DBC1 promotes castration-resistant prostate cancer by positively regulating DNA binding and stability of AR-V7

Sue Jin Moon1,2, Byong Chang Jeong3, Hwa Jin Kim1,2

  • 1Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul, Korea.

Oncogene
|December 19, 2017
PubMed

Insights

DBC1 acts as a coactivator for androgen receptor variant 7 (AR-V7), enhancing its DNA binding and stability. This discovery is crucial for understanding and treating castration-resistant prostate cancer (CRPC) progression.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cancer Research

Background:

  • Androgen receptor variant 7 (AR-V7) is a key driver of castration-resistant prostate cancer (CRPC) and anti-androgen resistance.
  • Regulatory mechanisms of AR-V7 transcriptional activity remain incompletely understood.

Purpose of the Study:

  • To identify and characterize novel regulators of AR-V7 transcriptional activity and stability in CRPC.
  • To elucidate the role of DBC1 in AR-V7 function and CRPC progression.

Main Methods:

  • Cell-based assays to assess AR-V7 transcriptional activity and stability.
  • Chromatin immunoprecipitation (ChIP) assays to evaluate AR-V7 recruitment to enhancers.
  • Co-immunoprecipitation assays to study protein-protein interactions.
  • CRPC cell line models to evaluate the impact of DBC1 depletion on tumorigenic and metastatic properties.

Main Results:

  • DBC1 acts as a coactivator for AR-V7, promoting the expression of target genes like CDH2.
  • DBC1 facilitates AR-V7 recruitment to target enhancers and chromatin looping.
  • DBC1 enhances AR-V7 DNA-binding activity and protects AR-V7 from CHIP E3 ligase-mediated degradation.
  • Depletion of DBC1 significantly suppresses the tumorigenic and metastatic potential of CRPC cells.

Conclusions:

  • DBC1 is a critical coactivator of AR-V7, regulating its DNA binding and stability.
  • DBC1 plays a significant physiological role in CRPC progression.
  • Targeting DBC1 may represent a novel therapeutic strategy for CRPC.

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