METTL3-mediated m6A modification promotes processing and maturation of to facilitate nasopharyngeal carcinoma cell proliferation and invasion.

The interplay between N6-methyladenosine (m6A) modification and microRNAs (miRs) participates in cancer progression. This study is conducted to explore the role of in nasopharyngeal carcinoma (NPC) cell proliferation and invasion. Reverse transcription quantitative polymerase chain reaction and Western blot showed that was upregulated in NPC tissues and cells and related to poor prognosis, methyltransferase-like 3 (METTL3) was highly expressed, whereas BMP and activin membrane-bound inhibitor () was weakly expressed in NPC tissues and cells. downregulation inhibited cell proliferation and invasion, whereas overexpression played the opposite role. m6A quantification and m6A RNA immunoprecipitation assays showed that METTL3-mediated m6A modification promoted the processing and maturation of via DiGeorge syndrome critical region gene 8 (DGCR8). Dual-luciferase assay showed that was a target of . The rescue experiments showed that downregulation reversed the role of inhibition in NPC cells. A xenograft tumor model showed that METTL3 downregulation inhibited tumor growth via the in vivo. Overall, our findings elicited that METTL3-mediated m6A modification facilitated the processing and maturation of via DGCR8 to upregulate , and inhibited expression to promote NPC cell proliferation and invasion, thus driving NPC progression.