Induction of autophagy by dimethyl cardamonin is associated with proliferative arrest in human colorectal carcinoma HCT116 and LOVO cells
- Induction of autophagy by dimethyl cardamonin is associated with proliferative arrest in human colorectal carcinoma HCT116 and LOVO cells
- 고현석; 김영주; Evangeline C. Amor; Jong Wha Lee; 김한천; 김희주; 양현옥
- Dimethyl cardamonin; Autophagy; G2/M cell cycle arrest; HCT116; LOVO
- Issue Date
- Journal of cellular biochemistry
- VOL 112, NO 9, 2471-2479
- 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.
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