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<p>Hepatocellular carcinoma (HCC) is a highly heterogeneous, proliferative, and aggressive malignancy of the digestive system. MicroRNAs (miRNAs) are expected to be a new target for the treatment of HCC. Crosstalk between N6-methyladenine (m6A) modification and miRNAs are involved in HCC progression. This study aimed to explore the role of miR-1293 and its underlying mechanism in HCC progression. The biological behaviors of HCC cells were analyzed by cell counting kit-8 and transwell assay. The underlying mechanism was determined by quantitative real-time PCR, methylated RNA immunoprecipitation (MeRIP), RIP, and xenograft tumor experiment. The results indicated that miR-1293 was highly expressed in HCC. Upregulated miR-1293 promoted the viability, invasion, and migration of HCC cells. Mechanically, the level of METTL3 and m6A modification was increased in HCC cells. METTL3 accelerated the processing and maturation of pri-miR-1293 in an m6A-dependent manner. Moreover, miR-1293 mimic reversed the inhibitory effect of METTL3 knockdown on HCC cellular biological behaviors. In addition, miR-1293 promoted tumor growth in vivo. This study revealed the regulatory role of miR-1293 in HCC is related to the participation of METTL3-mediated m6A methylation, which could provide new therapeutic strategies for HCC.</p>

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MiRNA- 1293 Promotes Hepatocellular Carcinoma Cell Proliferation and Invasion by METTL3-Mediated m6 A Modification of Pri-miRNA- 1293

  • 期刊论文

  • 发表日期：

    2025年4月28日

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  • Jingwen Liu,
  • Beibe Zhu,
  • Nenglie Jin,
  • Jie Lv,
  • Hongke Zhou

摘要

Hepatocellular carcinoma (HCC) is a highly heterogeneous, proliferative, and aggressive malignancy of the digestive system. MicroRNAs (miRNAs) are expected to be a new target for the treatment of HCC. Crosstalk between N6-methyladenine (m6A) modification and miRNAs are involved in HCC progression. This study aimed to explore the role of miR-1293 and its underlying mechanism in HCC progression. The biological behaviors of HCC cells were analyzed by cell counting kit-8 and transwell assay. The underlying mechanism was determined by quantitative real-time PCR, methylated RNA immunoprecipitation (MeRIP), RIP, and xenograft tumor experiment. The results indicated that miR-1293 was highly expressed in HCC. Upregulated miR-1293 promoted the viability, invasion, and migration of HCC cells. Mechanically, the level of METTL3 and m6A modification was increased in HCC cells. METTL3 accelerated the processing and maturation of pri-miR-1293 in an m6A-dependent manner. Moreover, miR-1293 mimic reversed the inhibitory effect of METTL3 knockdown on HCC cellular biological behaviors. In addition, miR-1293 promoted tumor growth in vivo. This study revealed the regulatory role of miR-1293 in HCC is related to the participation of METTL3-mediated m6A methylation, which could provide new therapeutic strategies for HCC.