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<p>m6A modifications are involved in regulating microRNA (miRNA) processing and maturation, and are associated with tumor development. Therefore, this study was aimed to explore the mechanism of miR-122-5p in regulating hepatocellular carcinoma (HCC) progression. mRNA expression and transfection efficiency were detected by RT-qPCR. Western blot was employed to measure protein level. Cell functions were evaluated through CCK-8 and transwell, respectively. Intracellular m6A levels were analyzed by MeRIP. Dual luciferase reporter gene, RIP and co-IP were applied to verify the binding relationship. Xenograft tumor model was carried out for in vivo validation of miR-122-5p function. We reported that miR-122-5p was clearly lessened in HCC. Functionally, miR-122-5p introduction inhibited the malignant progression of HCC. Mechanistically, METTL14 insertion promoted miR-122-5p maturation by labeling pri-miR-122 with m6A. In addition, miR-122-5p exerted suppressor effects by targeting Lysine acetyltransferase 2&#xa0;A(KAT2A). Moreover, we also found that KAT2A overexpression limited β-catenin expression through succinylation modification. Finally, animal data also illustrated that miR-122-5p introduction could hinder the growth of HCC tumors in vivo. We revealed the existence of a METTL14/miR-122-5p/KAT2A/β-catenin mechanistic axis in HCC, which has not been reported in the literature. This newly discovered mechanistic axis may provide new ideas for HCC therapy.</p>

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METTL14-mediated miR-122-5p maturation stimulated tumor progression by targeting KAT2A in hepatocellular carcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月23日

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  • Xiangyu Fan,
  • Wenjuan Qiao,
  • Xu Guo,
  • Jiaqi Wang,
  • Lisong Zhao

摘要

m6A modifications are involved in regulating microRNA (miRNA) processing and maturation, and are associated with tumor development. Therefore, this study was aimed to explore the mechanism of miR-122-5p in regulating hepatocellular carcinoma (HCC) progression. mRNA expression and transfection efficiency were detected by RT-qPCR. Western blot was employed to measure protein level. Cell functions were evaluated through CCK-8 and transwell, respectively. Intracellular m6A levels were analyzed by MeRIP. Dual luciferase reporter gene, RIP and co-IP were applied to verify the binding relationship. Xenograft tumor model was carried out for in vivo validation of miR-122-5p function. We reported that miR-122-5p was clearly lessened in HCC. Functionally, miR-122-5p introduction inhibited the malignant progression of HCC. Mechanistically, METTL14 insertion promoted miR-122-5p maturation by labeling pri-miR-122 with m6A. In addition, miR-122-5p exerted suppressor effects by targeting Lysine acetyltransferase 2 A(KAT2A). Moreover, we also found that KAT2A overexpression limited β-catenin expression through succinylation modification. Finally, animal data also illustrated that miR-122-5p introduction could hinder the growth of HCC tumors in vivo. We revealed the existence of a METTL14/miR-122-5p/KAT2A/β-catenin mechanistic axis in HCC, which has not been reported in the literature. This newly discovered mechanistic axis may provide new ideas for HCC therapy.