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The critical roles of N 6 -methyladenosine (m 6 A) modification have been demonstrated by more and more evidence. However, the cross talk of m 6 A and long noncoding RNAs (lncRNAs) in non-small cell lung cancer (NSCLC) tumorigenesis is still unclear. Here, this work focused on the functions and molecular mechanism of m 6 A-modified lncRNA DLGAP1 antisense RNA 2 (DLGAP1-AS2) in NSCLC. Microarray analysis found that lncRNA DLGAP1-AS2 is upregulated in NSCLC cells. Clinical data showed that DLGAP1-AS2 high-expression was correlated with advanced pathological stage and poor prognosis. Functionally, DLGAP1-AS2 overexpression promoted the aerobic glycolysis and DLGAP1-AS2 knockdown suppressed the tumor growth of NSCLC cells. Mechanistically, m 6 A methyltransferase METTL3 enhanced the stability of DLGAP1-AS2 via m 6 A site binding. Moreover, DLGAP1-AS2 interacted with YTHDF1 to enhance the stability of c-Myc mRNA through DLGAP1-AS2/YTHDF1/m 6 A/c-Myc mRNA. In conclusion, our work indicates the functions of m 6 A-modified DLGAP1-AS2 in the NSCLC aerobic glycolysis, disclosing a potential m 6 A-dependent manner for NSCLC treatment.

METTL3-induced DLGAP1-AS2 promotes non-small cell lung cancer tumorigenesis through m 6 A/c-Myc-dependent aerobic glycolysis