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Diallyl disulfide (DADS), a major organosulfur compound of garlic oil, is known to have an anticancer effect on human cancer cells. However, the exact mechanisms of this anticancer activity remain unclear. Here, we investigate the effects of DADS on cell cycle progression in human colon cancer HCT-116 cells by exploring the role played by regulatory molecules such as p53 and cyclin B1. Treatment of HCT-116 cells by DADS induced a marked growth inhibition with a slight reduction in viability and induced transient cell cycle arrest in the G2/M phase. Cyclin B1 is thought to play an important role in this process, as the DADS-induced G2/M phase arrest occurs with the increase of cyclin B1 expression. DADS also significantly induced the expression of p53, which contributes to cell cycle arrest in cancer cells, at a late time-point of 24 h. In addition, knockdown of p53 by siRNA did not affect cell cycle arrest, its reversibility, or the expression of cyclin B1 in the G2/M phase induced by DADS. Based on these results we conclude that, with the dynamic expression of cyclin B1, DADS induces reversible cell cycle arrest in the G2/M phase of HCT-116 cells through a p53-independent mechanism.

Agaricus blazei is well known as a traditional medicinal mushroom and it has been shown to exhibit immunostimulatory and anti-cancer activity. However, the cellular and molecular mechanism of cell cycle arrest and apoptosis of cancer cells is poorly understood. In this study, we have investigated whether A. blazei extract (ABE) exerts anti-proliferative and apoptotic effects on human gastric epithelial AGS cells. It was found that ABE could inhibit cell growth in a dose-dependent manner, which was associated with the arrest of G2/M phase and the induction of apoptotic cell death. Flow cytometric analysis showed that ABE could cause an arrest at the G2/M phase of the cell cycle, which is closely correlated to decreased cyclin B1 and cdc2 levels. Furthermore, this compound induced apoptosis through up-regulation of Bax and the activation of caspases with down-regulation of XIAP and cIAP-1, but not cIAP-2, and a capase-3 inhibitor could block cell death and apoptotic body formation. These data clearly indicate that ABE-induced apoptosis is associated with caspase-3 activation. In summary, the growth inhibition of ABE is highly related to cell cycle arrest at the G2/M phase and the induction of caspase-3-dependent apoptosis in human gastric epithelial AGS cells.