Stud Y Of Metformin Activatin G AMPK Pathway And Inhibitin G PD-L1 Expression In The Development Of Gastric Cancer

Background: Gastric cancer is a common gastrointestinal tumor in general surgery with high morbidity and mortality.The main treatment strategies are radical resection and chemo-radiotherapy,but the mortality is still high in China.Metformin,a common hypoglycemic drug,has been found to reduce the risk of several cancers includes lung,breast,prostate,endometrial and colorectal cancers.This study aims to find some possible mechanisms of how metformin affect gastric cancer,which may apply in gastric cancer therapy.Methods: Gastric cancer cells(SGC-7901)were treated with cultures contained in different concentrations of metformin and observed the growth of gastric cancer cells.Control group cells were cultured with RPMI-1640.CCK8 was used to calculate the survival of gastric cells.Wound healing and transwell assay were used to evaluate the migration ability of gastric cells.We analyzed the standards of E-cadherin and N-cadherin,the EMT-associated proteins,through western blot.Western blot were used to analysis the standard of T-AMPK,P-AMPK,PD-L1.The changes of PD-L1 and its m RNA were detected after the regulation of AMPK pathway by western blot and RT-PCR.The changes of AMPK pathway were detected after the silencing of PD-L1 by western blot.Results: CCK8 showed the survival of gastric cells goes down in the metformin(P<0.05).Wound healing and transwell assay found that metformin inhibit the migration of gastric cells.E-cadherin and N-cadherin,which are EMT-associated proteins,were suppressed by metformin(P<0.05).Western blot detected that the AMPK pathway was stimulated by metformin,and the standard of PD-L1 was suppressed(P<0.05).Once AMPK was knocked down,PD-L1 would increase(P<0.05).O nce PD-L1 slinced,AMPK did not change(P>0.05).Conclusions: Metformin inhibits proliferation and migration of gastric cancer and suppress the PD-L1 through stimulate AMPK pathway.