Fig. 1

IGF2BPs regulate R-loop metabolism in an m6A-dependent manner, leading to inhibition of cell migration and growth retardation in PCa. A Without IGF2BPs, YTHDF2 preferentially binds to R-loops containing m6A, leading to the elimination of R-loops. DNMT1 binds directly to the promoter of SEMA3F, forming CpG islands and inhibiting SEMA3F transcription. B IGF2BPs selectively bind to m6A-modified R-loops and cause R‑loop accumulation. IGF2BPs also upregulate SEMA3F expression via repelling DNMT1 and YTHDF2. SEMA3s, the expression products of SEMA3F, activate the Hippo pathway and inhibit tumorigenesis, angiogenesis, and tissue growth suppression