Objective To investigate the impact of dipeptidyl peptidase 3 (DPP3) on the immune escape of gastric cancer cells by regulating the expression of major histocompatibility complex class I chain-related gene B (MICB). Methods Knocking down DPP3 in MKN-45 human gastric cancer cells and overexpressing DPP3 in MGC-803 human gastric cancer cells, observing changes in cell proliferation, migration ability, and responses to natural killer (NK) cell cytotoxicity; using whole-transcriptome sequencing to identify the MICB gene, and knocking down MICB in DPP3-overexpressing cells to verify changes in cellular behavior. In C57 mice, the in vivo tumorigenic ability of DPP3-knockout cells and the infiltration of CD56 cells in tissues were examined.
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