TRIM25 facilitates ferroptosis in ovarian cancer through promoting PIEZO1 K63-linked ubiquitination and degradation

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Ya Li1, Fei Zhou1, Zhengmei Xu1

  • 1Department of Gynecology, Affiliated Hengyang Hospital of Hunan Normal University & Hengyang Central Hospital, Hengyang, No.12 Yancheng Road, Hengyang city, Hunan province, 421000, PR China.

Translational Oncology
|April 18, 2025
PubMed
Abstract

Insights

TRIM25 promotes ovarian cancer by degrading PIEZO1, inhibiting ferroptosis, and driving cell proliferation. Targeting TRIM25 or PIEZO1 may offer new ovarian cancer treatment strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cellular Biology

Background:

  • Ovarian cancer is a major threat to women's health.
  • Ferroptosis is a potential cancer inhibitor, but TRIM25's role in ovarian cancer and ferroptosis regulation is unknown.

Purpose of the Study:

  • To investigate the mechanism of TRIM25 in ovarian cancer.
  • To explore TRIM25's potential role in regulating ferroptosis for cancer therapy.

Main Methods:

  • Functional gain- and loss-of-function assays (in vitro and in vivo).
  • Identification of TRIM25 target genes.
  • Analysis of PIEZO1 stability and ubiquitination sites via protein docking and ubiquitination experiments.

Main Results:

  • TRIM25 is highly expressed in ovarian cancer, promoting tumor growth and metastasis.
  • TRIM25 targets PIEZO1 for ubiquitination-dependent degradation.
  • TRIM25 inhibits ferroptosis, thereby stimulating ovarian cancer cell proliferation.

Conclusions:

  • TRIM25 stimulates ovarian cancer by inducing K63-linked ubiquitination of PIEZO1, suppressing ferroptosis and promoting proliferation.
  • Identification of the PIEZO1 ubiquitination site offers potential therapeutic targets for ovarian cancer.
Keywords:
FerroptosisOvarian cancerTRIM25

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