Scholarlink

Background <p>Gastric cancer (GC) is a highly malignant cancer worldwide. UBE2N, a key E2 ubiquitin ligase, regulates protein ubiquitination and plays a crucial role in cancer progression. The course of GC is intimately linked to anomalies in the p53 pathway. Therefore, this study explored the mechanism of UBE2N in GC, especially its regulation of p53 degradation.</p> Methods <p>This study used a variety of experimental methods to explore the mechanism of UBE2N in the progression of GC. By constructing UBE2N knockdown and overexpression GC cell models, Western blot analysis was used to detect the effect of UBE2N on p53 protein levels. ROS levels, lipid peroxidation, and cell viability were assessed, and the UBE2N-p53 interaction was confirmed via co-immunoprecipitation (Co-IP).</p> Results <p>Knockdown of UBE2N reduced GC cell viability, promoted apoptosis by modulating pro- and anti-apoptotic proteins, and enhanced ferroptosis by altering oxidative stress markers and ferroptosis regulators. Mechanistically, UBE2N knockdown stabilized p53 by reducing its ubiquitination, thereby activating p53-mediated tumor suppressor pathways. Downregulation of p53 reversed the pro-apoptotic and pro-ferroptotic effects of UBE2N knockdown.</p> Conclusion <p>This study identified UBE2N as a key regulatory factor in GC, which provides a favorable environment for tumor growth by inhibiting p53-mediated apoptosis and ferroptosis. Targeting UBE2N to restore p53 function may become a new therapeutic strategy to help inhibit the development of GC and improve patient prognosis.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

UBE2N is associated with gastric cancer progression: inhibiting apoptosis and ferroptosis by mediating p53 degradation

  • 期刊论文

  • 发表日期：

    2025年9月27日

查看全文
  • Chai Hua,
  • Shuang Jiang,
  • Yanfeng Li,
  • Jingjing Qian,
  • Zhiyong Shen

摘要

Background

Gastric cancer (GC) is a highly malignant cancer worldwide. UBE2N, a key E2 ubiquitin ligase, regulates protein ubiquitination and plays a crucial role in cancer progression. The course of GC is intimately linked to anomalies in the p53 pathway. Therefore, this study explored the mechanism of UBE2N in GC, especially its regulation of p53 degradation.

Methods

This study used a variety of experimental methods to explore the mechanism of UBE2N in the progression of GC. By constructing UBE2N knockdown and overexpression GC cell models, Western blot analysis was used to detect the effect of UBE2N on p53 protein levels. ROS levels, lipid peroxidation, and cell viability were assessed, and the UBE2N-p53 interaction was confirmed via co-immunoprecipitation (Co-IP).

Results

Knockdown of UBE2N reduced GC cell viability, promoted apoptosis by modulating pro- and anti-apoptotic proteins, and enhanced ferroptosis by altering oxidative stress markers and ferroptosis regulators. Mechanistically, UBE2N knockdown stabilized p53 by reducing its ubiquitination, thereby activating p53-mediated tumor suppressor pathways. Downregulation of p53 reversed the pro-apoptotic and pro-ferroptotic effects of UBE2N knockdown.

Conclusion

This study identified UBE2N as a key regulatory factor in GC, which provides a favorable environment for tumor growth by inhibiting p53-mediated apoptosis and ferroptosis. Targeting UBE2N to restore p53 function may become a new therapeutic strategy to help inhibit the development of GC and improve patient prognosis.