Related Experiment Video

Updated: May 1, 2026

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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USP13 promotes enzalutamide resistance by catalyzing depolyubiquitination of PCMT1 in prostate cancer

Zhipeng Wang1,2,3, Xiaoqiang Liu1,2, Zhongqi Li1,2

  • 1Department of Urology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.

Cell Death & Disease
|April 29, 2026
PubMed

Insights

Targeting USP13, a deubiquitinating enzyme, can overcome enzalutamide resistance in prostate cancer. USP13 inhibition reduces tumor growth and enhances treatment efficacy by suppressing PCMT1.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Castrate-resistant prostate cancer (CRPC) often develops resistance to therapies like enzalutamide due to androgen receptor (AR) pathway activation.
  • Deubiquitinating enzymes (DUBs) are implicated in cancer progression and represent potential therapeutic targets.

Purpose of the Study:

  • To investigate the role of the DUB USP13 in prostate cancer (PCa) progression and enzalutamide resistance.
  • To explore USP13 as a therapeutic target for overcoming treatment resistance in CRPC.

Main Methods:

  • Analysis of USP13 expression in PCa tissues.
  • In vitro and in vivo studies involving USP13 silencing in PCa cells.
  • Investigation of the interaction between USP13 and PCMT1.
  • Assessment of enzalutamide sensitivity following USP13 inhibition.

Main Results:

  • USP13 is upregulated in PCa tissues and correlates with disease progression.
  • USP13 silencing inhibits PCa cell growth in vitro and in vivo.
  • USP13 stabilizes PCMT1 by removing polyubiquitination, promoting PCa proliferation and enzalutamide resistance.
  • USP13 inhibition sensitizes PCa cells to enzalutamide and reduces tumor growth via PCMT1 suppression.

Conclusions:

  • USP13 plays a critical role in promoting PCa cell proliferation and resistance to enzalutamide.
  • USP13 inhibition represents a promising therapeutic strategy to overcome enzalutamide resistance in prostate cancer, particularly in cases with USP13/PCMT1 overexpression.

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