Fig. 3
From: Biological and pharmacological roles of m6A modifications in cancer drug resistance
m6A-regulated oncogenic bypass signaling. Downregulation of ALKBH5 led to the downregulation of WIF-1 mRNA expression, thus activating the Wnt pathway. The elevated levels of m6A in circRNA-SORE enhanced its stability and allowed it to competitively activate the Wnt/β-certain pathway by acting as a miRNA sponge. YTHDC2 promoted radiotherapy resistance by activating the IGF1R-AKT/S6 signaling axis. m6A modification-mediated DUXAP8 contributed to chemoresistance via miR-584-5p/MAPK1/ERK. Chidamide decreased c-MET expression and increased crizotinib sensitivity by reducing m6A methylation. NKAP promoted SLC7A11 mRNA splicing and maturation, thereby inhibiting ferroptosis