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N  6 -methyladenosine (m 6 A) is the most common epigenetic RNA modification with essential roles in cancer progression. However, roles of m 6 A and its regulator METTL3 on non-coding RNA in gastric cancer are unknown. In this study, we found elevated levels of m 6 A and METTL3 in gastric cancer. Increased METTL3 expression indicated poor outcomes of patients and high malignancy in vitro and in vivo. Mechanically, m 6 A facilitated processing of pri-miR-17-92 into the miR-17-92 cluster through an m 6 A/DGCR8-dependent mechanism. The m 6 A modification that mediated this process occurred on the A879 locus of pri-miR-17-92. The miR-17-92 cluster activated the AKT/mTOR pathway by targeting  PTEN  or  TMEM127 . Compared with those with low levels of METTL3, METTL3-high tumors showed preferred sensitivity to an mTOR inhibitor, everolimus. These results reveal a perspective on epigenetic regulations of non-coding RNA in gastric cancer progression and provide a theoretical rationale for use of everolimus in the treatment of m 6 A/METTL3-high gastric cancer.

N6-methyladenosine-dependent pri-miR-17-92 maturation suppresses PTEN/TMEM127 and promotes sensitivity to everolimus in gastric cancer