Fig. 4From: Interaction between N6-methyladenosine modification and the tumor microenvironment in colorectal cancerm6A modifications interact with the CRC inflammatory microenvironment. METTL3 promotes the formation of the inflammatory microenvironment and CRC proliferation by inhibiting SOCS2. Additionally, METTL3 promotes M1-type macrophage polarization and inhibits M2-type macrophage by promoting STAT1 expression. The m6A methylated EphA2/VEGFA promotes angiogenesis in CRC by targeting the PI3K/AKT inflammatory signaling pathway. The functions of m6A “erasers” in the inflammatory microenvironment of CRC are still unclearBack to article page