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In MM, CD4 + and CD8 + T-cells form the primary immune defense, however, tumor-induced remodeling of the TME is unfavorable to T-cells due to nutrient deprivation, acidosis, and the accumulation of toxic metabolites (146) ( Figure 1 )

Furthermore, METTL3 can promote gastric carcinogenesis by activating the METTL3/m6A/miR-1184 axis via an m6A-dependent mechanism, thereby interfering with the miR-1184/TRPM2 signaling pathway (34).Recent findings indicate that the demethylase ALKBH5, which regulates ZKSCAN3 expression via N 6 -methyladenosine (m 6 A) modification, activates VEGFA transcription and facilitates MNNG-induced gastric cancer cell migration, invasion, cancer stem cell (CSC) generation, vasculogenic mimicry (VM), and ultimately, gastric cancer progression (13)

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doi: 10.1007/BF00686114