IGF2BP3 boosts lactate generation to accelerate gastric cancer immune evasion.

The CD8 T cells mediated antitumor immunity plays a critical function on gastric cancer (GC) immunotherapy. However, the mechanism of N-methyladenosine (mA) and lactate in GC immune microenvironment are still unclear. Here, present research investigated the role of Insulin like growth factor II mRNA binding protein 3 (IGF2BP3) in GC and its in-depth mechanisms in the antitumor immunity.

N-methyladenosine (mA) reader IGF2BP1 accelerates gastric cancer aerobic glycolysis in c-Myc-dependent manner.

The N-methyladenosine (mA) is involved in the regulation of cell proliferation and metastasis formation in multiple cancers. However, the biological significance of RNA mA reader IGF2BP1 and the modification of IGF2BP1 itself have not been fully investigated. Here, we analyzed the functions and mechanism of IGF2BP1 in gastric cancer (GC).