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Journal of Cancer Prevention

Original Article

Journal of cancer prevention 2013; 18(1): 33-40

Published online March 30, 2013

© Korean Society of Cancer Prevention

Anticancer Mechanism of AP1, Abalone Peptide by Cell Cycle Arrest in Human Gastric Cancer Cells

Cho Won Kim1*, Hye-Jin Go2*, Jung-Kil Seo3, Nam Gyu Park2 and Gun-Do Kim1

Abstract

Gastric cancer is one of the most common malignant tumors and the second cause of cancer related death in the world. Here, we evaluated the effects of abalone peptide (AP1) on cellular mediators involved in cell cycle arrest in gastric cancer cells. AGS and MKN-28 cell lines were used as human gastric cancer cells and the mechanism study showed that AP1 decreased cell population by cell cycle arrest and then led to apoptotic cell death of MKN-28 and AGS cells. Cell cycles were analyzed by flow cytometry and western blotting. Treatment with AP1 arrested the cell cycle in G1/S phase. AP1 decreased expressions of not only CDK2 and CDK6 but also Cyclin D1 and Cyclin D3. Along with those decrease, expressions of phospho-Rb, E2F1, phospho-chk1 and Cdc25A also decreased as well. Activation of caspases-3, -6 and -7 was also observed. In conclusion, the findings in this study suggested that AP1 have potential anticancer efficacy via cell cycle arrest in G1/S phase and induction of apoptosis. Its potential role to be a candidate of anticancer agent is worth being further investigated. (Cancer Prev Res 18, 33-40, 2013)

Keywords: Abalone peptide, Gastric cancer cells, MKN-28, AGS, Cell cycle, Apoptosis

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