Related Experiment Video

Updated: Jul 20, 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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ESS2 controls prostate cancer progression through recruitment of chromodomain helicase DNA binding protein 1

Sayuri Takahashi1,2, Ichiro Takada3,4, Kenichi Hashimoto5

  • 1Department of Urology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-Ku, Tokyo, 108-8639, Japan. t-sayuri@athena.ocn.ne.jp.

Scientific Reports
|July 31, 2023
PubMed

Insights

The transcriptional coregulator ESS2 drives prostate cancer growth and progression. Targeting ESS2 offers a novel epigenetic therapeutic strategy for castration-resistant prostate cancer (CRPC).

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Poly (ADP-ribose) polymerase inhibitors improved survival in castration-resistant prostate cancer (CRPC) but are only effective in patients with specific mutations.
  • There is a need for novel drug discovery targeting epigenetic modulators for CRPC treatment.

Purpose of the Study:

  • To investigate the role of the transcriptional coregulator ESS2 in prostate cancer.
  • To evaluate ESS2 as a potential therapeutic target for CRPC.

Main Methods:

  • ESS2 knockdown in PC3 cells and subsequent tumor xenograft studies in nude mice.
  • Microarray analysis to identify ESS2-regulated genes.
  • Chromatin immunoprecipitation assays to assess protein recruitment and histone modifications.
  • Analysis of prostate development in tamoxifen-inducible Ess2-knockout mice.

Main Results:

  • ESS2 knockdown significantly inhibited prostate cancer cell proliferation in vivo.
  • ESS2 regulates key cancer-related genes, including those involving chromodomain helicase DNA binding protein 1 (CHD1), PPAR-γ, WNT5A, and TGF-β.
  • ESS2 knockdown reduced nuclear factor (NF)-κB/CHD1 recruitment and H3K36me3 levels at target gene promoters.
  • ESS2 enhances the transcriptional activity of NF-κB, NFAT, and SMAD2/3.
  • Ess2 deficiency in mice led to delayed prostate development and cellular abnormalities.

Conclusions:

  • ESS2 functions as a crucial transcriptional coregulator in prostate cancer.
  • ESS2 represents a promising novel epigenetic therapeutic target for castration-resistant prostate cancer (CRPC).

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