Morin enhances auranofin anticancer activity by up-regulation of DR4 and DR5 and modulation of Bcl-2 through reactive oxygen species generation in Hep3B human hepatocellular carcinoma cells.

摘要: Evidence suggests that auranofin (AF) exhibits anticancer activity by inhibiting thioredoxin reductase (TrxR). Here, in this study, we have investigated the synergistic effects of AF and morin their mechanism for focusing on apoptosis Hep3B human hepatocellular carcinoma cells. We assessed activities annexin V/PI double staining, caspase, TrxR assay. Morin enhances inhibitory as well reducing cell viability. Annexin staining revealed morin/AF cotreatment induced apoptotic death. AF-induced mitochondrial membrane potential (ΔΨm) loss cytochrome c release. Further, upregulated death receptor DR4/DR5, modulated Bcl-2 family members (upregulation Bax downregulation Bcl-2), activated caspase-3, -8, -9. also reactive oxygen species (ROS) generation. The results from caspase-dependent apoptosis, which was triggered via extrinsic pathway upregulating TRAIL receptors (DR4/DR5) enhanced intrinsic modulating inhibitor protein members. These are related to ROS In conclusion, study provides evidence can enhance cells, indicating its combination could be an alternative treatment strategy carcinoma.