Fig. 2: The interactions between m6A methylation and ncRNAs in PCa.

A METTL3 bound to DGCR8, identified the m6A site on pri-miR-182, promoted its maturation, and ultimately accelerated PCa invasion and migration. B VIRMA stabilized the expression of lncRNA CCAT1/CCAT2 by targeting its m6A site and promoted the proliferation and invasion of PCa. C METTL3 stabilized the expression of lncRNA SNHG7 through m6A modification, facilitated its binding with SRSF1, and ultimately increased the expression of c-MYC, thus promoting the proliferation and glycolysis of PCa. D METTL3 promoted the expression of lncRNA MALAT1 through m6A modification, thereby affecting the PI3K/AKT pathway and promoting the proliferation and invasion of PCa. E LncRNA NEAT1 can recruit CYCLINL1 and CDK19 to the promoter region of RUNX2 through m6A modification sites and promote PCa bone metastasis. F METTL3 can mediate lncRNA PCAT6 m6A modification, and then bind IGF2BP2 and IGF1R mRNA to form a complex to stabilize its expression, and ultimately promote PCa bone metastasis. G WTAP formed a complex with circPDE5A, bound to EIF3C, and ultimately down-regulated its expression, promoting PCa migration and invasion.