The m6A reader IGF2BP3 promotes LIHC progression by enhancing MCM10 stability

Abnormal N6-methyladenosine (m6A) modifications were associated with the occurrence, development, and metastasis of cancer. However, the functions and mechanisms of m6A regulators in cancer remained largely elusive and should be explored. Here, we identified that IGF2BP3 was specifically overexpressed and associated with poor prognosis in LIHC. Importantly, IGF2BP3 promoted liver hepatocellular carcinoma (LIHC) cell progression in an m6A-dependent manner, IGF2BP3 silencing significantly inhibited proliferation and migratory ability of tumor cells in vitro. Mechanistically, IGF2BP3 interacted with minichromosomal maintenance complex component (MCM10) mRNAs to prolong stability of m6A-modified RNA. Therefore, our findings indicated that m6A reader IGF2BP3 contributed to tumorigenesis and poor prognosis, providing a potential prognostic biomarker and therapeutic target for LIHC.