RBM10, a new potential RBP function, recruits METTL3 to induce N6-methyladenosine-MALAT1-dependent modification on inhibiting the invasion and migration of NSCLC

Background : Previous studies have shown that RBM10 is a potential tumor suppressor protein that can inhibit proliferation and promote apoptosis of NSCLC. RBM10 can bind and modify RNA at the post transcriptional level. Method and results : Transwell and cell wound healing assay showed that RBM10 significantly inhibited the invasion and migration of NSCLC. CLIP-seq showed that among all RBM10 binding RNAs, lncRNA MALAT1 with high m6A methylation in lung cancer had the highest binding peak among all non-coding RNAs. RNA Immunoprecipitation has verified the direct combination of RBM10 and MALAT1. The rescue experiment confirmed that RBM10 affected the phosphorylation of PI3K/AKT/mTOR passway protein, the invasion and migration ability by regulating MALAT1. MeRIP-qPCR confirmed that RBM10 could inhibit MALAT1 m6A methylation levels by recruiting METTL3. Conclusion : These results suggest that RBM10, as an RNA-binding protein, may inhibit m6A methylation of MALAT1 by recruiting METTL3, and affect phosphorylation of the downstream PI3K/AKT/mTOR pathway by binding and regulating MALAT1, ultimately affecting the invasion and migration of NSCLC.