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Lipid‐soluble extract of Red Ginseng inhibits the growth of lung cancer cells through induction of apoptosis and cell cycle arrest
Author(s) -
Kang Moo Rim,
Park Sung Kyu,
Kim Hwan Mook,
Lee Chang Woo,
Kim Dong Chung
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.lb500
Subject(s) - cell cycle , apoptosis , cyclin dependent kinase 6 , chemistry , cyclin dependent kinase , cell cycle checkpoint , cell growth , microbiology and biotechnology , biology , biochemistry
It is known that red ginseng has a lot of biological activities, including anti‐tumor activity. In this study we investigated the anticancer activity of lipid‐soluble ginseng extract (HRE) prepared by n‐hexane extraction. The inhibitory activity of HRE on the growth of NCI‐H460 human lung cancer cells was evaluated by the sulforhodamine B assay. The effect of HRE on apoptosis and cell cycle was also analyzed. HRE exhibited a potent antiproliferative effect against the NCI‐H460 cells and induced G0/G1 cell cycle arrest. The percentage of G0/G1 increased from 54.5 to 74.0%, but S phase decreased from 42.1 to 17.2%. HRE effectively reduced the level of cell cycle mediators, such as CDK,2, CDK4, CDK6, cyclin D3 and cyclin E, at the concentration of 100 ug/ml. In addition, HRE also induced apoptosis in these cells, which was accompanied by the activation of caspases, including caspase‐9, caspase‐8 and caspase‐3. The pan‐caspase inhibitor, Z‐VAD‐fmk, partially blocked the cell death induced by HRE. Our results indicate that HRE exerts an anti‐proliferative activity against lung cancer cells by perturbing the cell cycle and activating the caspase pathways.