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  • Title: [Role of autophagy on cobrotoxin induced cell death of A549].
    Author: Shen J, He J, Tang X, Han R, Li R, Xu C, Wu Y.
    Journal: Zhongguo Fei Ai Za Zhi; 2013 Jul; 16(7):339-44. PubMed ID: 23866663.
    Abstract:
    BACKGROUND: It has been proven that cobrotoxin has anti-tumor effect while its role in lung cancer is rarely studied. The aim of this study is to assay the anti-tumor effect of cobrotoxin in cell line A549, and also to explore its possible mechanism related to autophagy and P38-MARK pathway. METHODS: Using MTT method to observe the inhibition effect of cobrotoxin on the growth of adenocarcinoma cell A549 and human lung fibroblast cell HFL1, as well as on that of A549 pretreated with 3-MA and SB203580, which are the inhibitor of autophagy and P38-MARK pathway respectively. Cell colony tablet cloning experiment was executed to detect the effect of cobrotoxin on colony formation of A549. Determining the protein levels of beclin-1, LC3, p38 and pP38 in A549 by Western blot after cells were exposed to cobrotoxin, or to cobrotoxin combined with either 3-MA or SB203580. RESULTS: All of different concentrations of cobrotoxin inhibited the growth of A549, but had no obvious effect on that of HFL1. After treating with 3-MA or SB203580, the suppress effect of cobrotoxin on A549 reduced. What's more, different concentrations of cobrotoxin all significantly suppressed the colony formation of A549. The expression of beclin-1 and pP38 in A549 increased obviously after exposure to cobrotoxin, and also the ratio of LC3 II to LC3 I amplified with a dose-dependant manner, but P62 decreased. The protein level of beclin-1 and the ratio of LC3 II to LC3 I in cells pretreated with 3-MA were reduced, while that of p62 was increased. Also, in cells that treated with SB203580 before exposed to cobrotoxin, the expression of beclin-1, pP38 and the ratio of of LC3 II to LC3 I were reduced, but the expression of P62 increased. CONCLUSIONS: Cobrotoxin can suppress the growth of A549 in vitro. And the activating of P38-MARK pathway, then upregulating autophagy, was involved in cobrotoxin induced anti-tumor process. 背景与目的 已有的研究表明眼镜蛇神经毒素具有抗肿瘤作用，而其在肺癌中的作用罕有研究。本研究观察cobrotoxin对人肺A549腺癌细胞株的抗肿瘤作用，探讨自噬和P38-MAPK通路在这过程中的作用。方法 应用MTT法观察cobrotoxin对A549细胞和HFL1人肺成纤维细胞的生长抑制作用以及用3-MA抑制自噬、SB203580抑制P38-MAPK通路后cobrotoxin对A549细胞的生长抑制作用；应用细胞集落平板克隆实验检测cobrotoxin对A549细胞的集落形成的影响；蛋白免疫印迹法（Western blot）测定单独cobrotoxin作用、cobrotoxin分别联合3-MA抑制自噬和SB203580抑制P38-MAPK通路活性后A549细胞内beclin-1、LC3、P62、P38及pP38等蛋白表达水平。结果 不同浓度cobrotoxin对A549细胞的生长有明显抑制作用，对HFL1人肺成纤维细胞无明显抑制作用，3-MA、SB203580作用后cobrotoxin对A549细胞的抑制作用降低；不同浓度cobrotoxin可明显抑制A549细胞的集落形成；cobrotoxin作用后beclin-1、pP38蛋白表达水平明显提高，P62表达明显降低，II型/I型LC3比值增大，并有浓度依赖性，3-MA抑制自噬后beclin-1蛋白表达水平降低，P62表达增高、II型/I型LC3比值减小，SB203580抑制P38-MAPK通路后beclin-1、pP38蛋白表达水平降低，II型/I型LC3比值减小。结论 cobrotoxin对人肺A549腺癌细胞体外生长有抑制作用，可能通过活化P38-MAPK通路激活自噬参与抗肿瘤过程。
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