LMP2A inhibits the expression of KLF5 through the mTORC1 pathway in EBV-associated gastric carcinoma

• The expression of KLF5 was significantly reduced in EBV-associated gastric carcinoma tissues and cells compared with EBV-negative gastric carcinoma tissues and cells. • LMP2A downregulates KLF5 expression by inhibiting the mTORC1 pathway in EBVaGC cells. • KLF5 can enhance the migration ability of GC cells and induce autophagy. Objective: To investigate the expression and biological role of KLF5 in EBV-associated gastric carcinoma (EBVaGC) and EBV-negative gastric carcinoma (EBVnGC), and to clarify the relationship between EBV and KLF5. Methods: The expression of KLF5 in GC tissues was detected by immunohistochemistry. Western blot and immunofluorescence assay were used to examine the expression and localization of KLF5 in EBV positive and negative GC cell lines. The effect of LMP2A on KLF5 was analyzed by transfection of LMP2A plasmid or siRNA. The function of KLF5 in GC was elucidated by molecular biology experiments. Results : The expression of KLF5 was significantly reduced in EBVaGC tissues and cell lines. LMP2A inhibited KLF5 expression through inactivating mTORC1 pathway in EBV positive GC cell lines. Meanwhile, KLF5 could enhance the migration ability of GC cells and induce autophagy. Conclusion: LMP2A downregulated KLF5 expression by inhibiting the mTORC1 pathway in EBV positive GC cells. KLF5 might play an oncogene-like role by promoting the migration of GC cells and inducing autophagy.