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<p>Increasing evidence indicates that RNA-binding proteins and the reprogramming of lipid metabolism play crucial roles in tumorigenesis. However, the extent to which members of these families contribute, and whether targeting metabolic genes to affect overall protein production in cancer cells, remains largely unknown. This study analyzes CRC tissue samples and databases to reveal the high expression of hnRNP A1 in CRC and its critical role in tumorigenesis, proliferation, migration, and prognosis. Through combined sequencing analyses, we identified a novel mechanism by which PPARα regulates lipid metabolism. Our data indicate that hnRNP A1 is central to lipid metabolism reprogramming in CRC, promoting lipid accumulation by regulating PPARα mRNA stability, thereby influencing cell proliferation and apoptosis. Overall, hnRNP A1 could serve as a novel target for CRC therapy. Its involvement in cancer development offers new biological insights and potential therapeutic strategies. As a potential biomarker and therapeutic target, it presents novel approaches for the clinical management of CRC.</p>

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hnRNP A1 inhibits colorectal cancer tumorigenesis and progression by regulating fatty acid metabolism and RNA stability

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月24日

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  • Kai Ji,
  • Leqi Zhou,
  • Tianshuai Zhang,
  • Hao Fan,
  • Gang Xie,
  • Wenjiang Man,
  • Can Wang,
  • Yucheng Tian,
  • Li Chen,
  • Guimin Wang,
  • Mulin Liu,
  • Bing Zhu,
  • Wei Zhang,
  • Guanyu Yu

摘要

Increasing evidence indicates that RNA-binding proteins and the reprogramming of lipid metabolism play crucial roles in tumorigenesis. However, the extent to which members of these families contribute, and whether targeting metabolic genes to affect overall protein production in cancer cells, remains largely unknown. This study analyzes CRC tissue samples and databases to reveal the high expression of hnRNP A1 in CRC and its critical role in tumorigenesis, proliferation, migration, and prognosis. Through combined sequencing analyses, we identified a novel mechanism by which PPARα regulates lipid metabolism. Our data indicate that hnRNP A1 is central to lipid metabolism reprogramming in CRC, promoting lipid accumulation by regulating PPARα mRNA stability, thereby influencing cell proliferation and apoptosis. Overall, hnRNP A1 could serve as a novel target for CRC therapy. Its involvement in cancer development offers new biological insights and potential therapeutic strategies. As a potential biomarker and therapeutic target, it presents novel approaches for the clinical management of CRC.