Induction of autophagy by dimethyl cardamonin is associated with proliferative arrest in human colorectal carcinoma HCT116 and LOVO cells
| Autor: | Young-Joo Kim, Hyeonseok Ko, Hee Ju Kim, Han-Cheon Kim, Evangeline C. Amor, Jong Wha Lee, Hyun Ok Yang |
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| Rok vydání: | 2011 |
| Předmět: |
Autophagosome
Programmed cell death Chalcone ATG5 Cell Gene Expression Antineoplastic Agents Apoptosis Cell Cycle Proteins Biology Biochemistry Autophagy-Related Protein 5 chemistry.chemical_compound Chalcones Autophagy medicine Humans Molecular Biology Cell Proliferation Cell growth Adenine Membrane Proteins Cell Cycle Checkpoints Cell Biology HCT116 Cells Cell biology medicine.anatomical_structure chemistry Cancer research Beclin-1 RNA Interference Apoptosis Regulatory Proteins Colorectal Neoplasms Microtubule-Associated Proteins |
| Zdroj: | Journal of Cellular Biochemistry. 112:2471-2479 |
| ISSN: | 0730-2312 |
| DOI: | 10.1002/jcb.23171 |
| Popis: | 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 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. J. Cell. Biochem. 112: 2471–2479, 2011. © 2011 Wiley-Liss, Inc. |
| Databáze: | OpenAIRE |
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