Envafolimab inhibits the growth of AGS gastric cancer cells by down-regulating SLC1A3/ERK/MAPK signaling pathway
Objective To investigate the effect of envafolimab on the proliferation,invasion and migration of AGS gastric cancer cells and its mechanism.Methods AGS cells were cultured in vitro and divided into envafolimab groups(2.5,5,10,20 and 40mg/ml of envafolimab,respectively)and control group(equal volume of normal saline).Cell viability was detected by cell counting kit-8(CCK8)assay,cell invasion and migration were detected by Transwell assay,and cell apoptosis was detected by flow cytometry.The differential proteins and related signaling pathways of the two groups were analyzed by proteomics,and the differential proteins and pathways found were verified by Western blot.Results Compared with the control group,the survival rate of AGS cells was significantly decreased in the envafolimab group(P=0.0060).It also significantly inhibited the invasion and migration of AGS cells(P=0.0052),and promoted the apoptosis of AGS cells(P=0.0030).Cluster analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment revealed that solute carrier family 1 member 3(SLC1A3)protein expression was significantly down-regulated in the envafolimab group compared with the control group,which was related to the mitogen-activated protein kinase(MAPK)pathway.Western blot showed that the expression of SLC1A3 protein in AGS cells treated with envafolimab was significantly decreased(P=0.0041),and the phosphorylation levels of mitogen-activated extracellular signal-regulated kinase(MEK)and extracellular signal-regulated kinase(ERK)were also significantly decreased(P=0.0008).Conclusion Envafolimab can inhibit the growth of AGS gastric cancer cells possibly by down-regulating the expression of SLC1A3 and inhibiting the ERK/MAPK signaling pathway.Multiple antitumor mechanisms of action are possible for envafolimab.
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