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

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.