Bostrycin inhibits proliferation of human lung carcinoma A549 cells via downregulation of the PI3K/Akt pathway |
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Authors: | Wei-Sheng Chen Jun-Na Hou Yu-Biao Guo Hui-Ling Yang Can-Mao Xie Yong-Cheng Lin Zhi-Gang She |
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Affiliation: | 1.Department of Pulmonary and Critical Care Medicine, the First Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510080, China;2.Department of Physiopathology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou 510080, China;3.Marine Microorganism Lab, Institute of Chemistry and Chemical Engineering, Sun Yat-Sen University, Guangzhou 510080, China |
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Abstract: | BackgroundBostrycin is a novel compound isolated from marine fungi that inhibits proliferation of many cancer cells. However, the inhibitory effect of bostrycin on lung cancers has not been reported. This study is to investigate the inhibitory effects and mechanism of bostrycin on human lung cancer cells in vitro.MethodsWe used MTT assay, flow cytometry, microarray, real time PCR, and Western blotting to detect the effect of bostrycin on A549 human pulmonary adenocarcinoma cells.ResultsWe showed a significant inhibition of cell proliferation and induction of apoptosis in bostrycin-treated lung adenocarcinoma cells. Bostrycin treatment caused cell cycle arrest in the G0/G1 phase. We also found the upregulation of microRNA-638 and microRNA-923 in bostrycin-treated cells. further, we found the downregulation of p110α and p-Akt/PKB proteins and increased activity of p27 protein after bostrycin treatment in A549 cells.ConclusionsOur study indicated that bostrycin had a significant inhibitory effect on proliferation of A549 cells. It is possible that upregulation of microRNA-638 and microRNA-923 and downregulaton of the PI3K/AKT pathway proteins played a role in induction of cell cycle arrest and apoptosis in bostrycin-treated cells. |
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