Scholarlink

<p>The deubiquitinating enzyme USP14, which belongs to the ubiquitin-specific protease family, is highly expressed in various malignant tumors. The regulatory mechanisms in tumors are complex and diverse, encompassing a range of cellular processes such as proliferation, apoptosis, inflammation, autophagy, and drug resistance. However, the functional role of USP14 in gastric cancer remains unclear. In the current investigation, a significant upregulation of USP14 expression was observed in gastric cancer, and its overexpression was associated with an unfavorable prognosis among patients. The involvement of USP14 is indispensable for promoting the growth, motility, and infiltration of gastric cancer cells, as revealed by our findings. Further investigations revealed that USP14 interacts with KPNA2 and is responsible for deubiquitinating it by removing ubiquitin. Moreover, the deubiquitylation process mediated by USP14 was found to be critically dependent on the K48 residue of ubiquitin. The knockdown of USP14 significantly suppressed the proliferation, migration, and invasion of gastric cancer cells. This effect was attributed to the regulation of c-MYC nuclear translocation through KPNA2 deubiquitination. The findings underscore the imperative for further evaluation of the potential therapeutic significance of USP14 in gastric cancer.</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

The deubiquitination enzyme USP14 promotes the tumourigenesis of gastric cancer by enhancing c-MYC nuclear translocation through deubiquitination of KPNA2

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月21日

查看全文
  • Jia Li,
  • Houyi Tang,
  • Hongbo Chang,
  • Yi Du,
  • Liang Du,
  • Erhu Zhao

摘要

The deubiquitinating enzyme USP14, which belongs to the ubiquitin-specific protease family, is highly expressed in various malignant tumors. The regulatory mechanisms in tumors are complex and diverse, encompassing a range of cellular processes such as proliferation, apoptosis, inflammation, autophagy, and drug resistance. However, the functional role of USP14 in gastric cancer remains unclear. In the current investigation, a significant upregulation of USP14 expression was observed in gastric cancer, and its overexpression was associated with an unfavorable prognosis among patients. The involvement of USP14 is indispensable for promoting the growth, motility, and infiltration of gastric cancer cells, as revealed by our findings. Further investigations revealed that USP14 interacts with KPNA2 and is responsible for deubiquitinating it by removing ubiquitin. Moreover, the deubiquitylation process mediated by USP14 was found to be critically dependent on the K48 residue of ubiquitin. The knockdown of USP14 significantly suppressed the proliferation, migration, and invasion of gastric cancer cells. This effect was attributed to the regulation of c-MYC nuclear translocation through KPNA2 deubiquitination. The findings underscore the imperative for further evaluation of the potential therapeutic significance of USP14 in gastric cancer.