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Dicycloplatin,a new supramolecular platinum antitumor drug which was formed by one molecule carboplatin and one molecule 1,1-ring succinic acid via the effect of hydrogen bond.In this study,we investigated theanticancer activities and signaling pathways implicated in apoptosis which induced by dicycloplatin in cancer cells.Dicycloplatin indeed inhibited proliferation of cancer cells and increased the percentage of apoptotic ceils in a concentration-dependent manner.Moreover,the changes of mitochondrial pathway-related factors were detected,such as the collapse of mitochondrial membrane potential (△Ψm),release of cytochrome c from the mitochondria to the cytosol,activation of caspases including caspase-9,caspase-3,and poly (ADP-ribose) polymerase cleavage in a concentration-dependent manner.Furthermore,the changes of the Bcl-2 family were also detected,such as down-regulation of Bcl-2 and Bid and up-regulation of Bad.Interestingly,activation and the cleavage of caspase-8,a death receptor pathway-related caspase,were detected in cancer cells after treated with dicycloplatin,too.Additionally,dicycloplatin increased the generation of reactive oxygen species (ROS) in cancer cells.DNA intercalation was not involved in apoptosis induced by dicycloplatin.In conclusion,these findings suggest that mitochondrial pathway and death receptor pathway plays some role in apoptotic process induced by dicycloplatin.Moreover,we found that the effects ofdicycloplatin on cancer cells are similar to carboplatin.