[Dipeptidyl peptidase 3 (DPP3) inhibits immune escape of gastric cancer cells through down-regulation of major histocompatibility complex class I chain-related gene B (MICB) expression].

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. Results Knocking out DPP3 promoted the proliferation and migration of gastric cancer cells, reduced MICB expression, and made the cells less sensitive to NK cell cytotoxicity; the tumorigenic ability in mice increased and CD56 cells tissue infiltration decreased by DPP3 knocking out in the gastric cancer cells, but DPP3 overexpression showed the opposite results. Knocking down MICB could reverse the phenotypic changes induced by high DPP3 expression. Conclusion DPP3 inhibits the immune escape of gastric cancer cells by downregulating MICB expression.