Molecular mechanism of apoptosis induction in skin cancer cells by the centipedegrass extract

BMC Complementary and Alternative Medicine

Research Article

Hyoung-Woo Bai¹  Byung Yeoup Chung¹  Srilatha Badaboina¹  Bo Yun Choi¹  Dong Min Jang²  Chul-Hong Park² 

[1] Advanced Radiation Technology Institute (ARTI), Korea Atomic Energy Research Institute (KAERI), Jeongeup-si, 580-185, Jeollabuk-do, Republic of Korea;Advanced Radiation Technology Institute (ARTI), Korea Atomic Energy Research Institute (KAERI), Jeongeup-si, 580-185, Jeollabuk-do, Republic of Korea;School of Biological Sciences and Biotechnology, Chonnam National University, 500-757, Gwangju, Republic of Korea;

关键词: Centipedegrass extract;    Apoptosis;    B16F1;    SKMEL-5;    PI3K/AKT/GSK-3β;    Caspase;    Skin cancer;   

DOI  :  10.1186/1472-6882-13-350

 received in 2013-03-15, accepted in 2013-11-29,  发布年份 2013

来源: Springer

【 摘 要 】

BackgroundCentipedegrass extract (CGE) is mainly composed of maysin and its derivatives, which are recognized internationally as natural compounds. Compared to other flavonoids, maysin has a unique structure in that mannose is bound to the flavonoid backbone. CGE exhibits some biological properties in that it can function as an anti-oxidant, anti-inflammatory, anti-adipogenic, and insecticidal. Whether CGE has other biological functions, such as anti-cancer activity, is unknown.MethodsB16F1 (mouse) and SKMEL-5 (human) cells were treated with CGE, and their subsequent survival was determined using MTT assay. We performed a cell cycle analysis using propidium iodide (PI), and detected apoptosis using double staining with annexin V-FITC/PI. In addition, we examined mitochondrial membrane potentials using flow cytometry, as well as signaling mechanisms with an immunoblotting analysis.ResultsCGE inhibited skin cancer cell growth by arresting the cell cycle in the G2/M phase, and increased both early and late apoptotic cell populations without affecting normal cells. Furthermore, we observed mitochondrial transmembrane depolarization, increased cytochrome-c release, caspase-3 and caspase-7 activation, and increased poly ADP-ribose polymerase degradation. CGE also downregulated activation of p-AKT, p-glycogen synthase kinase-3β (GSK-3β), and p-BAD in a time-dependent manner. LY294002 inhibition of phosphoinositide 3-kinase (PI3K) significantly sensitized skin cancer cells, which led to an increase in CGE-induced apoptosis.ConclusionsCGE controlled skin cancer cell growth by inhibiting the PI3K/AKT/GSK-3β signaling pathway and activating the effector caspases. This study is the first to demonstrate anti-cancer properties for CGE, and that CGE may be an effective therapeutic agent for treating skin cancer.

【 授权许可】

Unknown   
© Badaboina et al.; licensee BioMed Central Ltd. 2013. This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.