Induction of autophagy by dimethyl cardamonin is associated with proliferative arrest in human colorectal carcinoma HCT116 and LOVO cells

Title
Induction of autophagy by dimethyl cardamonin is associated with proliferative arrest in human colorectal carcinoma HCT116 and LOVO cells
Authors
고현석김영주Evangeline C. AmorJong Wha Lee김한천김희주양현옥
Keywords
Dimethyl cardamonin; Autophagy; G2/M cell cycle arrest; HCT116; LOVO
Issue Date
2011-09
Publisher
Journal of cellular biochemistry
Citation
VOL 112, NO 9, 2471-2479
Abstract
Dimethyl cardamonin (20,40-dihydroxy-60-methoxy-30,50-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 DMC on cell proliferation, cell-cycle distribution, and programmed cell death in cultures of human colorectal carcinoma HCT116 and LOVO cells. Results showed that DMC inhibited HCT116 and LOVO cell proliferation and induced G2/M cell cycle arrest, which was associated with the conversion of microtubule associated protein light chain 3 (LC3)-I–LC3-II, an autophagosome marker, and the incorporation of monodansylcadaverine (MDC), a marker for the acidic compartment of autolysosomes or acidic vesicular organelles. The treatment of HCT116 and LOVO cells using a 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 anti-proliferation. These results imply that DMC can suppress colorectal carcinoma HCT116 and LOVO cell proliferation through a 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 HCT116 and LOVO colorectal carcinoma cells.
URI
http://pubs.kist.re.kr/handle/201004/40577
ISSN
0730-2312
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