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.
Xing et al. (Wed,) studied this question.