Scholarlink

<p>Colon cancer (CC) is a common malignancy with rising incidence worldwide. Despite advances in treatment strategies, many patients still face a poor prognosis due to the development of drug resistance. Long non-coding RNAs (lncRNAs) have emerged as important regulators of various biological processes and have been implicated in cancer progression. Among them, colorectal neoplasia differentially expressed (CRNDE) has drawn attention for its potential roles in different cancers. However, its specific functions in CC remain unclear. In this study, we identified CRNDE as highly expressed in CC, contributing to tumor progression and drug resistance. Mechanically, CRNDE is regulated by the transcription factor TFAP2A. Additionally, CRNDE inhibits pyroptosis, a form of programmed cell death, by promoting the ubiquitin-mediated degradation of RIPK3, thereby reducing the sensitivity of CC cells to 5-fluorouracil (5-FU). Our findings suggest that the TFAP2A/CRNDE/RIPK3 axis plays critical roles in colon cancer progression and chemoresistance, highlighting potential therapeutic targets for improving treatment outcomes.</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

TFAP2A-regulated CRNDE enhances colon cancer progression and chemoresistance via RIPK3 interaction

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年2月15日

查看全文
  • Xin Gao,
  • Yanming Huang,
  • Tonghui Wei,
  • Jingmin Xue,
  • Filippov Iurii,
  • Laishou Yang,
  • Liying Wang,
  • Hao Li,
  • Genshen Mo,
  • Yuze Huang,
  • Haonan Xie,
  • Hang Wang,
  • Shenghan Lou,
  • Peng Han

摘要

Colon cancer (CC) is a common malignancy with rising incidence worldwide. Despite advances in treatment strategies, many patients still face a poor prognosis due to the development of drug resistance. Long non-coding RNAs (lncRNAs) have emerged as important regulators of various biological processes and have been implicated in cancer progression. Among them, colorectal neoplasia differentially expressed (CRNDE) has drawn attention for its potential roles in different cancers. However, its specific functions in CC remain unclear. In this study, we identified CRNDE as highly expressed in CC, contributing to tumor progression and drug resistance. Mechanically, CRNDE is regulated by the transcription factor TFAP2A. Additionally, CRNDE inhibits pyroptosis, a form of programmed cell death, by promoting the ubiquitin-mediated degradation of RIPK3, thereby reducing the sensitivity of CC cells to 5-fluorouracil (5-FU). Our findings suggest that the TFAP2A/CRNDE/RIPK3 axis plays critical roles in colon cancer progression and chemoresistance, highlighting potential therapeutic targets for improving treatment outcomes.