SDF-1CXCR4-PI3K信号通路对乳腺癌细胞MDA-MB-231增殖与凋亡的影响.docVIP

精品论文 参考文献 SDF-1CXCR4-PI3K信号通路对乳腺癌细胞MDA-MB-231增殖与凋亡的影响 易敏 　　（湘潭职业技术学院外科教研室湖南湘潭411101） 　　【摘要】目的：探讨SDF-1/CXCR4-PI3K信号通路对乳腺癌增殖和凋亡的影响，为临床治疗乳腺癌提供新的思路和方法。方法：以乳腺癌MDA-MB-231细胞系为研究对象，通过免疫细胞化学、MTT比色法、软琼脂克隆形成实验、流式细胞仪等方法检测经SDF-1/CXCR4-PI3K信号通路特异性阻断剂AMD3100和LY294002分别处理及联合处理后，MDA-MB-231细胞增殖和凋亡能力的变化。结果：免疫细胞化学检测结果表明，乳腺癌MDA-MB-231细胞表达CXCR4蛋白。AMD3100抑制剂不影响CXCR4蛋白表达，LY294002抑制剂下调p-AKT蛋白表达。MTT比色法和软琼脂克隆形成实验证实MDA-MB-231细胞经AMD3100、LY29400或AMD3100+LY294002作用后其增殖能力与对照组相比较明显降低(P＜005，n=5)。流式细胞仪检测细胞周期和细胞凋亡结果表明，MDA-MB-231细胞在AMD3100、LY29400或AMD3100+LY294002作用下其DNA复制停滞于G2/M期，并且出现明显的“亚二倍体”凋亡峰，其凋亡率明显高于对照组(P＜001，n=3)。结论：AMD3100和LY294002可抑制乳腺癌细胞的增殖能力，促进凋亡。SDF-1/CXCR4-PI3K信号通路可能以抑制细胞凋亡的形式参与了肿瘤的形成过程，是参与乳腺癌细胞增殖的一条重要信号转导途径。为临床治疗乳腺癌提供了新的思路和方法。 　　【关键词】SDF-1/CXCR4-PI3K；MDA-MB-231乳腺癌细胞Effect of SDF-1/CXCR4-PI3K signal pathway on proliferation and apoptosis of breast cancer cell line MDA-MB-231 　　Yi Min(Xiangtan Vocational and Technical College Department of surgery, Hunan, Xiangtan, 411101) 　　【Abstract】Objective: To investigate the effect of SDF-1/CXCR4-PI3K signal pathway on proliferation and apoptosis of breast cancer, to provide new ideas and methods for the treatment of breast cancer. Methods: The breast cancer MDA-MB-231 cell line as the research object, by immunocytochemistry, MTT colorimetric assay, soft agar colony formation assay, flow cytometry method via SDF-1/CXCR4-PI3K pathway specific inhibitor AMD3100 and LY294002 respectively and combined treatment, change in the ability of proliferation and apoptosis of MDA-MB-231 cells. Results: The results of immunocytochemistry assay showed that, the expression of CXCR4 in breast cancer cell line MDA-MB-231. AMD3100 inhibitors do not affect the protein expression of CXCR4, LY294002 inhibitors reduced expression of p-AKT protein. MTT assay and soft agar colony formation assay demonstrated that MDA-MB-231 cells treated with AMD3100, LY29400 or AMD3100+LY294002 after their proliferation ability compared with the control group decreased significantly (Plt;