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<p>Endometrial cancer (EC) is a malignant tumor originating from the uterine epithelial lining and is one of the most common gynecologic malignancies worldwide. Ubiquitination, as a crucial regulatory mechanism in cell physiology, plays a key role in processes such as cell cycle control, DNA repair, and tumorigenesis. UPF1, a critical regulator of ubiquitination, is involved in the development of various diseases, including cancer, due to its influence on mRNA stability and protein degradation. This study aims to identify novel molecular targets related to EC pathogenesis and to explore their mechanisms of action. Through bioinformatics analysis, we identified ZNF432 as a significantly differentially expressed gene in EC tissues. Functional experiments demonstrated that ZNF432 overexpression significantly inhibited EC cell proliferation and induced apoptosis. In in vivo experiments, ZNF432 overexpression significantly suppressed tumor growth in a nude mouse xenograft model. Mechanistically, ZNF432 induced apoptosis by interacting with UPF1 and enhancing its ubiquitination, promoting the degradation of pro-survival factors in EC cells. These findings provide new insights into the molecular mechanisms underlying EC and highlight ZNF432 as a potential therapeutic target, offering promising prospects for the development of novel treatments.</p>

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ZNF432 suppresses endometrial cancer progression by promoting UPF1 ubiquitination and inducing apoptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月14日

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  • Xinjun Li,
  • Jie Qi,
  • Ren Xu,
  • Shuo Xu,
  • Shengpu Wang,
  • Chunxiao Wang,
  • Sufen Zhao

摘要

Endometrial cancer (EC) is a malignant tumor originating from the uterine epithelial lining and is one of the most common gynecologic malignancies worldwide. Ubiquitination, as a crucial regulatory mechanism in cell physiology, plays a key role in processes such as cell cycle control, DNA repair, and tumorigenesis. UPF1, a critical regulator of ubiquitination, is involved in the development of various diseases, including cancer, due to its influence on mRNA stability and protein degradation. This study aims to identify novel molecular targets related to EC pathogenesis and to explore their mechanisms of action. Through bioinformatics analysis, we identified ZNF432 as a significantly differentially expressed gene in EC tissues. Functional experiments demonstrated that ZNF432 overexpression significantly inhibited EC cell proliferation and induced apoptosis. In in vivo experiments, ZNF432 overexpression significantly suppressed tumor growth in a nude mouse xenograft model. Mechanistically, ZNF432 induced apoptosis by interacting with UPF1 and enhancing its ubiquitination, promoting the degradation of pro-survival factors in EC cells. These findings provide new insights into the molecular mechanisms underlying EC and highlight ZNF432 as a potential therapeutic target, offering promising prospects for the development of novel treatments.