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<p>WT1-associated protein (WTAP)-catalyzed m6A methylation drives oncogenic processes in HCC. Long noncoding RNA UNC5B-AS1 are associated with various types of cancer including hepatocellular carcinoma (HCC). Previous study indicated that UNC5B-AS1 promotes HCC progression. However, the precise roles of WTAP/UNC5B-AS1 axis in HCC progression remain unclear. In this study, we found that the m6A modification sites are highly abundant on UNC5B-AS1, and methylase WTAP enhances UNC5B-AS1 stability through m6A reader-YTHDF1 and up-regulates its expression in HCC. Functional tests showed that WTAP/UNC5B-AS1 axis drives HCC progression. Mechanically, UNC5B-AS1 acts as a molecular sponge to hsa-miR-760, to up-regulate the expression of Interleukin-6 (IL6), and plays a role in enhancing HCC progression. Our study reveals a mechanism by which m6A-RNA regulates oncogene activity, which might result in the creation of a therapeutic strategy for the treatment of HCC.</p>

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m6A modification-mediated lncRNA UNC5B-AS1 enhances HCC progression through miR-760/IL6 axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月24日

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  • Li-ping Yu,
  • Sheng-yu Huang,
  • Kun-peng Li,
  • Jun-sheng Ni,
  • Zhi-ping Huang,
  • Zhou-feng Deng

摘要

WT1-associated protein (WTAP)-catalyzed m6A methylation drives oncogenic processes in HCC. Long noncoding RNA UNC5B-AS1 are associated with various types of cancer including hepatocellular carcinoma (HCC). Previous study indicated that UNC5B-AS1 promotes HCC progression. However, the precise roles of WTAP/UNC5B-AS1 axis in HCC progression remain unclear. In this study, we found that the m6A modification sites are highly abundant on UNC5B-AS1, and methylase WTAP enhances UNC5B-AS1 stability through m6A reader-YTHDF1 and up-regulates its expression in HCC. Functional tests showed that WTAP/UNC5B-AS1 axis drives HCC progression. Mechanically, UNC5B-AS1 acts as a molecular sponge to hsa-miR-760, to up-regulate the expression of Interleukin-6 (IL6), and plays a role in enhancing HCC progression. Our study reveals a mechanism by which m6A-RNA regulates oncogene activity, which might result in the creation of a therapeutic strategy for the treatment of HCC.