Cell Cycle Arrest and Apoptotic Induction by MCS-C2 in Human Leukemia HL-60 Cells

The purpose of the present study was to investigate the anti-proliferative and apoptotic effects of MCS-C2, a novel analogue of toyocamycin and sangivamycin, in human promyelocytic leukemia (HL-60) cells. When treated with MCS-C2, inhibited proliferation associated with cell cycle arrest and apoptotic induction was found in the HL-60 cells in a concentration-dependent and time-dependent manner. This apoptotic induction was associated with the cleavage of Bid and a release of cytochrome c from mitochondria into the cytosol, followed by the activation of caspase-3 and inactivation of poly (ADP-ribose) polymerase (PARP). However, there was no significant change in any other mitochondrial membrane proteins, such as Bcl-2 and Bax. Consequently, the current findings suggest that the mitochondrial pathway was primarily involved in the MCS-C2-induced apoptosis in the human promyelocytic leukemia HL-60 cells.