Dimethyl cardamonin induces G2/M-phase cell cycle arrest, apoptosis and autophagy in HCT116 cells
- Dimethyl cardamonin induces G2/M-phase cell cycle arrest, apoptosis and autophagy in HCT116 cells
- 고현석; 김영주; 박진수; Evangeline C. Amor; 이종화; 양현옥
- Dimethyl cardamonin; autophagy; colorectal cancer
- Issue Date
- AACR (American Association for Cancer Research) 101st Annual Meeting 2010
- Dimethyl cardamonin (2’,4’-dihydroxy-6’-methoxy -3’,5’-dimethylchalcone; DMC) is a naturally occurring chalcone, and it is the major compound isolated from the leaves of Syzygium samarangense (Blume) Merr. & L.M. Perry (Myrtaceae). Experiments were conducted to determine the effects of a DMC on cell proliferation, cell-cycle distribution and programmed cell death in cultures of human HCT116 colorectal carcinoma cells. In this study, the effect of a DMC on the proliferation and autophagy of cultured HCT116 was elucidated. Results showed that DMC inhibited HCT116 cell proliferation and induced G2/M cell cycle arrest which was associated with the conversion of microtubule associated protein light chain 3 (LC3)-I to LC3-II, an autophagosome marker, and the incorporation of monodansylcadaverine (MDC), a marker for the acidic compartment of autolysosomes acidic vesicular organelles. Combination of DMC with an autophagy inhibitor, such as 3-methyladenine (3-MA), beclin 1 siRNA or ATG5 siRNA, suppressed the effect of DMC-mediated cell death. These results imply that DMC can suppress HCT116 colorectal carcinoma cells proliferation through G2/M phase cell-cycle delay, and can induce autophagy, the hallmark of Type II programmed cell death (PCD). Taken together, our results suggest that DMC may be an effective chemotherapeutic agent for colorectal
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