D-鼠李糖β常春藤甙通过抑制PI3K/AKT信号通路诱导乳腺癌细胞株MCF-7?MDA-MB-231凋亡
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国家自然科学基金资助(81272916);江苏省自然科学基金资助(BK2011855)


D-Rhamnose β hederin induces apoptosis of breast cancer cell lines MCF-7 and MDA-MB-231 by inhibiting PI3K/AKT signaling pathway
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    摘要:

    目的:观察D-鼠李糖β常春藤甙(简称D药)对乳腺癌细胞的杀伤作用,通过研究其对PI3K/AKT信号通路的影响,探索其抗肿瘤机制-方法:不同浓度D药作用于乳腺癌细胞株MCF-7-MDA-MB-231 48 h后,流式细胞仪Annexin V-FITC/PI双染法检测细胞凋亡率,Western blot 法检测D药作用MCF-7-MDA-MB-231后PI3K/AKT信号通路相关分子的蛋白表达-结果:20-30-40 -滋g/ml D药作用细胞48 h后可以诱导细胞凋亡,凋亡率随浓度升高而增加-20 -滋g/ml D药作用细胞48 h后,p-PI3K-p-AKT蛋白表达减少,而总PI3K-总AKT蛋白的表达量无明显变化-PI3K 抑制剂LY294002通过抑制细胞p-AKT的表达,从而增加D药引起的细胞凋亡-结论:D药可以通过抑制PI3K的磷酸化,进而影响磷酸化AKT的表达,最终诱导乳腺癌细胞凋亡-

    Abstract:

    Objective:To study the effect of D-Rhamnose β hederin on the apoptosis of breast cancer cells and its effect on PI3K/AKT signaling pathway to explore its antineoplastic mechanisms. Methods:Breast cancer cell lines MCF-7 and MDA-MB-231 were treated with D-Rhamnose β hederin at different concentrations. Apoptosis rate of MCF-7 and MDA-MB-231 after treated with D-Rhamnose β hederin for 48 h were analyzed by AnnexinV/PI double staining of flow cytometry. Protein expression of PI3K/AKT signaling pathway related molecules after treated with D-Rhamnose β hederin were detected by Western blot. Results:D-Rhamnose β hederin with dosage of 20,30,40 -滋g/ml effectively induced cell apoptosis and the apoptosis rate was increased with the rising concentration. After treatment with 20 -滋g/ml D-Rhamnose β hederin for 48 h,the protein expressions of p-PI3K and p-AKT were decreased,but the total expressions of PI3K and AKT were not significantly changed. Futhermore,PI3K inhibitor LY294002 enhanced D-Rhamnose β hederin-induced apoptosis through inhibition of p-AKT. Conclusion:D-Rhamnose β hederin could effect on the expression of AKT phosphorylation and significantly induce the apoptpsis of breast cancer cells by inhibiting the phosphorylation of PI3K.

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成琳,夏添松,周文斌,梁秀清,薛金秋,石靓,王莹,丁强. D-鼠李糖β常春藤甙通过抑制PI3K/AKT信号通路诱导乳腺癌细胞株MCF-7?MDA-MB-231凋亡[J].南京医科大学学报(自然科学版),2014,(4):446-451

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  • 收稿日期:2013-10-10
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  • 在线发布日期: 2014-04-18
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