TRIM8 promotes ovarian cancer proliferation and migration by targeting VDAC2 for ubiquitination and degradation

Sep 21, 2026

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Ovarian cancer is a common gynecological malignancy with high malignancy potential and poor prognosis. The study investigates TRIM8, an E3 ubiquitin ligase implicated in multiple tumors, and clarifies its regulatory role in ovarian cancer. Bioinformatics identified TRIM8 upregulation, and TRIM8 expression in tissues was evaluated by immunofluorescence. TRIM8 knockdown or overexpression in ovarian cancer cells assessed proliferation and migration using CCK8, transwell, and clonal assays, with in vivo effects measured by subcutaneous tumors in nude mice.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages16

Reading Time40 min

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Abstract

Background

Aims

Materials and Methods

Results

Discussion and Conclusion

Keywords

Introduction

DOI: 10. 1002/cam4 .7396 RESEAR CH ARTICLE TRIM8 promotes ovarian cancer proliferation and migration by targeting VDAC2 for ubiquitination and degradation Fei Wu1 | Jiaqi Xu1 | Xin Jin1 | Yue Zhu2 | Wenxin Gao3 | Meng Liu1 | Yan Zhang1 | Weifeng Qian2 | Xiaoyan Huang3 | Dan Zhao4,5 | Guannan Feng1 | Shunyu Hou1 | Xiaoxue Xi1 1Department of Obstetrics and Gynecology, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, China 2Department of Breast and Thyroid Surgery, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou Municipal Hospital, Suzhou, Jiangsu, China 3Department of Histology and Embryology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, China 4Reproductive Medicine Center, The Fourth Affiliated Hospital of Jiangsu University, Zhenjiang, China 5Institute of Reproductive Sciences, Jiangsu University, Zhenjiang, China Correspondence Guannan Feng, Shunyu Hou, and Xiaoxue Xi, Department of Obstetricsand Gynecology, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou Municipal Hospital, Suzhou 215002, Jiangsu, China. Email: [804750802@qq.com](804750802@qq.com), [houshunyu@sina.com](houshunyu@sina.com), and [xixiaoxue@126.com](xixiaoxue@126.com) Funding information Science and Technology Project of Suzhou of Jiangsu Province, Grant/ Award Number: SYS2020175; “Science and Education Revitalize Health”Youth Science and Technology Project of Suzhou, Grant/Award Number: KJXW2020028; Scientific Research Project of Gusu School of Nanjing Medical University, Grant/ Award Number: GSKY20210203 and GSKY20210208; Cultivation Special Project of Gusu School of Nanjing Medical University, Grant/Award Number: GSKY20220522; Special Abstract Background: Ovarian cancer is a common gynecological tumor with high malignant potential and poor prognosis. TRIM8, is involved in the development of various tumors, but its precise regulatory role in ovarian cancer is still unknown. Aims: The aim of this study was to explore the specific mechanism by which TRIM8 regulates ovarian cancer. Materials and Methods: We used bioinformatics analysis to screen for high expression of TRIM8 in ovarian cancer. The expression of TRIM8 in healthy and cancerous ovarian tissues was assessed by immunofluorescence. TRIM8 was silenced or overexpressed in ovarian cancer cell lines, with cell proliferation and migration evaluated by CCK8, transwell and clonal formation assays. The effect of TRIM8 on ovarian cancer cells in vivo was assessed by subcutaneous tumor formation experiments in nude mice. The potential interacting protein VDAC2 was identified by mass spectrometry. The mechanism underlying TRIM8 regulation ofVDAC2 was evaluated by co-immunoprecipitation and western blotting. Results: TRIM8 was overexpressed in ovarian cancer. TRIM8 promoted the proliferation and migration of ovarian cancer cells in vitro and the growth of subcutaneous tumors in mice in vivo. TRIM8 interacted with VDAC2, weakened the stability of the protein, and promoted its polyubiquitination and subsequent | Fei Wu, Jiaqi Xu, and Xin Jin contributed equally to this work. | | --- | | This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
© 2024 The Author(s). Cancer Medicine published by John Wiley & Sons Ltd. | Cancer Medicine. 2024;13:e7396 . [https://doi.org/10.1002/cam4.7396](https://doi.org/10.1002/cam4.7396) [wileyonlinelibrary.com/journal/cam4](wileyonlinelibrary.com/journal/cam4) 1 of 16 project of diagnosis and treatment technology for key clinical diseases of Suzhou of Jiangsu Province, Grant/ Award Number: LCZX202013; Key Research Foundation of Zhenjiang Social Develop

FAQs

What is the main research question about TRIM8 in ovarian cancer?

The study aims to determine the specific mechanism by which TRIM8 regulates ovarian cancer.

How did the researchers evaluate TRIM8 expression and its effects on ovarian cancer cells?

They screened for TRIM8 high expression by bioinformatics, measured TRIM8 in tissues using immunofluorescence, and tested TRIM8 knockdown or overexpression in cell lines. Proliferation and migration were assessed with CCK8, transwell, and clonal formation assays.

What role does VDAC2 play in the TRIM8-mediated pathway?

TRIM8 interacted with VDAC2, reduced VDAC2 protein stability, and increased its polyubiquitination and degradation. VDAC2 knockdown increased resistance of ovarian cancer cells to iron death, while VDAC2 overexpression attenuated ovarian cancer progression driven by TRIM8.

Sep 21, 2026

Uploaded by Violet