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Updated: Dec 4, 2025

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
12:13

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients

Published on: November 19, 2019

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Identification of AR-V7 downstream genes commonly targeted by AR/AR-V7 and specifically targeted by AR-V7 in

Masahiro Sugiura1, Hiroaki Sato1, Atsushi Okabe2

  • 1Department of Urology, Graduate School of Medicine, Chiba University, Chiba, Japan; Department of Molecular Oncology, Graduate School of Medicine, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba, Japan.

Translational Oncology
|October 23, 2020
PubMed

Insights

Androgen receptor variant 7 (AR-V7) drives castration-resistant prostate cancer (CRPC) progression by activating target genes, including NUP210 and SLC3A2. Silencing these genes suppresses CRPC cell growth, offering potential therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Prostate cancer (PC) can become castration-resistant (CRPC) during treatment.
  • Androgen receptor (AR) splice variant 7 (AR-V7) expression is a mechanism for CRPC development.

Purpose of the Study:

  • To investigate the role of AR-V7 in CRPC progression.
  • To identify AR-V7 target genes and their impact on CRPC cell growth.

Main Methods:

  • Comparative epigenome and transcriptome analyses of PC and CRPC cell lines.
  • Chromatin immunoprecipitation sequencing (ChIP-seq) to identify AR-V7 target regions.
  • Gene knockdown experiments and cell growth assays.

Main Results:

  • Identified 399 AR-V7 target regions, with 22 specifically bound by AR-V7.
  • Found 78 genes near AR-V7 targets highly expressed in CRPC cells; AR-V7 knockdown repressed these genes and suppressed LNCaP95 cell growth.
  • Upregulated NUP210 and SLC3A2 in CRPC tissues; their knockdown inhibited LNCaP95 cell growth via apoptosis and arrest.

Conclusions:

  • AR-V7 promotes CRPC proliferation by regulating both common and specific target genes.
  • NUP210 and SLC3A2 are key AR-V7 targets that contribute to CRPC growth and represent potential therapeutic targets.
Keywords:
AR-V7Androgen receptor (AR)Castration-resistant prostate cancer (CRPC)NUP210SLC3A2

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