期刊论文详细信息
BMC Complementary and Alternative Medicine
Molecular mechanism of apoptosis induction in skin cancer cells by the centipedegrass extract
Byung Yeoup Chung2  Bo Yun Choi2  Dong Min Jang1  Chul-Hong Park1  Hyoung-Woo Bai2  Srilatha Badaboina2 
[1] School of Biological Sciences and Biotechnology, Chonnam National University, Gwangju 500-757, Republic of Korea;Advanced Radiation Technology Institute (ARTI), Korea Atomic Energy Research Institute (KAERI), Jeongeup-si, Jeollabuk-do 580-185, Republic of Korea
关键词: Skin cancer;    Caspase;    PI3K/AKT/GSK-3β;    SKMEL-5;    B16F1;    Apoptosis;    Centipedegrass extract;   
Others  :  1220456
DOI  :  10.1186/1472-6882-13-350
 received in 2013-03-15, accepted in 2013-11-29,  发布年份 2013
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【 摘 要 】

Background

Centipedegrass 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.

Methods

B16F1 (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.

Results

CGE 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.

Conclusions

CGE 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】

   
2013 Badaboina et al.; licensee BioMed Central Ltd.

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