文章摘要
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,2014,(4):446~451
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
D-Rhamnose β hederin induces apoptosis of breast cancer cell lines MCF-7 and MDA-MB-231 by inhibiting PI3K/AKT signaling pathway
投稿时间:2013-10-10  
DOI:10.7655/NYDXBNS20140409
中文关键词: D-鼠李糖β 常春藤甙  乳腺癌  凋亡  PI3K/AKT
英文关键词: D-Rhamnose β hederin  breast cancer  apoptosis  PI3K/AKT
基金项目:国家自然科学基金资助(81272916);江苏省自然科学基金资助(BK2011855)
作者单位
成琳 南京医科大学第一附属医院乳腺外科,江苏 南京 210029 
夏添松 南京医科大学第一附属医院乳腺外科,江苏 南京 210029 
周文斌 南京医科大学第一附属医院乳腺外科,江苏 南京 210029 
梁秀清 南京医科大学第一附属医院乳腺外科,江苏 南京 210029 
薛金秋 南京医科大学第一附属医院乳腺外科,江苏 南京 210029 
石靓 南京医科大学第一附属医院乳腺外科,江苏 南京 210029 
王莹 南京医科大学第一附属医院乳腺外科,江苏 南京 210029 
丁强 南京医科大学第一附属医院乳腺外科,江苏 南京 210029 
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中文摘要:
      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?
英文摘要:
      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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