Studies on gypenosides-induced apoptosis of colorectal cancer cells by activating Atgl
Objective To investigate the inhibitory effect of gypenosides(Gyp)on colorectal cancer HCT116 cells and elucidate its underlying mechanisms.Methods Cell counting kit-8(CCK-8)assay and flow cytometry were used to detect Gyp′s effects on cell viability,cell cycle distribution,and apoptosis rate.The expression levels of mRNA and protein were detected by quantitative real time polymerase chain reaction(qRT-PCR)and western blot,respectively.The number of lipid droplets was detected by Bodipy staining.Results Gyp demonstrated the dose-and time-dependent inhibition of HCT116 cell proliferation.Gyp significantly induced G0/G1 phase cell cycle arrest,down-regulated cyclin-dependent kinases(CDKs,including CDK2,CDK4,and CDK6)proteins,and up-regulated p21 and p27 proteins.Gyp significantly increased cell apoptosis rate,and elevated Cleaved caspase-3,Cleaved Poly(ADP-ribose)polymerase 1(Cleaved PARP1),and Bcl-2 associated X protein(Bax)protein expressions,and decreased B cell lymphoma-xl(Bcl-xl)protein levels.Gyp also decreased lipid droplet formation,down-regulated fatty acid synthase(Fasn)mRNA,and up-regulated adipose triglyceride lipase(Atgl)mRNA and protein levels.Compared with Gyp alone treatment,the combination of Gyp and Atglisatin(Atgli,an adipose triglyceride lipase inhibitor)significantly increased the number of lipid droplets,with a concurrent reduction in apoptosis and Cleaved caspase-3 expression.Conclusion Gyp inhibits HCT116 cell proliferation by inducing cell cycle arrest and apoptosis.The mechanism involves the modulation of lipid metabolism mediated by Atgl.
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