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Updated: Jan 31, 2026

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel
06:44

Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel

Published on: September 8, 2017

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Targeting Ezh2 could overcome docetaxel resistance in prostate cancer cells

Xiaofu Qiu1,2, Wei Wang3, Bijun Li4

  • 1Department of Urology, Southern Medical University Third Medical College, Guangzhou, 510317, China. xfqiu123@163.com.

BMC Cancer
|January 10, 2019
PubMed
Abstract

Insights

Targeting EZH2 can overcome docetaxel resistance in prostate cancer. This study found EZH2 is induced in resistant cells, and blocking it suppresses cancer stem cells, offering a new therapeutic strategy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Docetaxel is a key treatment for metastatic castration-resistant prostate cancer (CRPC).
  • Docetaxel resistance in prostate cancer (PCa) limits its effectiveness.
  • Identifying mechanisms of resistance and new therapeutic targets is crucial.

Purpose of the Study:

  • To elucidate the mechanisms driving docetaxel resistance in prostate cancer.
  • To identify EZH2 as a potential therapeutic target for overcoming docetaxel resistance.

Main Methods:

  • Established docetaxel-resistant (DocR) prostate cancer cell lines.
  • Investigated the role of EZH2 by modulating its expression (overexpression) and activity (using an inhibitor).
  • Analyzed the impact of EZH2 inhibition on miRNA expression (miR-101-3p, miR-138-5p) and key stem cell markers (Nanog, Sox2, CD44).

Main Results:

  • EZH2 expression was upregulated in DocR cells, linked to suppressed miR-101-3p and miR-138-5p.
  • Inhibiting EZH2 activity or using miRNA mimics reversed docetaxel resistance.
  • EZH2 inhibition reduced docetaxel-induced cancer stem cell populations.
  • EZH2 activity was essential for the docetaxel-induced expression of Nanog, Sox2, and CD44.

Conclusions:

  • EZH2 is a critical mediator of docetaxel resistance in prostate cancer.
  • Targeting EZH2 presents a promising strategy to overcome docetaxel resistance.
  • Modulating EZH2 could be a novel therapeutic approach for treating resistant prostate cancer.

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