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<p>Hepatocellular carcinoma (HCC) is a globally prevalent and aggressive form of hepatic cancer. Both N<sup>6</sup>-methyladenosine (m<sup>6</sup>A) and long non-coding RNAs (lncRNAs) modification are identified as key mediators of HCC progression. However, comprehensive genome-wide studies and functional annotations of m<sup>6</sup>A-modified lncRNAs in HCC are still limited. In this study, LINC01315 demonstrated a significant increase in HCC and was closely associated with patient survival. <i>METTL3</i> was shown to increase LINC01315 expression by acting as its m<sup>6</sup>A methyltransferase, while <i>YTHDF1</i> served as the respective m<sup>6</sup>A reader. LINC01315 promoted the growth and metastatic ability of HCC. LINC01315 acts as a competing endogenous RNA (ceRNA) for miR-185-5p, which elevated β-catenin levels and activated the WNT signaling cascade in HCC cells. These findings highlight that <i>METTL3</i>-driven LINC01315 accelerates HCC cell propagation, invasion, and migration <i>via</i> the LINC01315/miR-185-5p/β-catenin/WNT signaling axis. LINC01315 could serve as a potent prognostic marker and treatment option in HCC.</p>

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N6-methyladenosine (m6A) of LINC01315 promotes hepatocellular carcinoma progression by activating β-Catentin/WNT pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月10日

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  • Ming-xuan Xing,
  • Bao-zhuang Sun,
  • Teng-yue Zou,
  • Ren-zheng Liu,
  • Guang-jin Li,
  • Wen-xiao Li

摘要

Hepatocellular carcinoma (HCC) is a globally prevalent and aggressive form of hepatic cancer. Both N6-methyladenosine (m6A) and long non-coding RNAs (lncRNAs) modification are identified as key mediators of HCC progression. However, comprehensive genome-wide studies and functional annotations of m6A-modified lncRNAs in HCC are still limited. In this study, LINC01315 demonstrated a significant increase in HCC and was closely associated with patient survival. METTL3 was shown to increase LINC01315 expression by acting as its m6A methyltransferase, while YTHDF1 served as the respective m6A reader. LINC01315 promoted the growth and metastatic ability of HCC. LINC01315 acts as a competing endogenous RNA (ceRNA) for miR-185-5p, which elevated β-catenin levels and activated the WNT signaling cascade in HCC cells. These findings highlight that METTL3-driven LINC01315 accelerates HCC cell propagation, invasion, and migration via the LINC01315/miR-185-5p/β-catenin/WNT signaling axis. LINC01315 could serve as a potent prognostic marker and treatment option in HCC.