摘要
研究了重组人血管内皮抑素(恩度)对雌激素受体阳性的人乳腺癌MCF-7细胞株生长的抑制作用与其分子机制.采用MTT法、台盼蓝染色法和中性红染色法检测不同浓度恩度对MCF-7细胞生长的抑制作用,Hoechst33258荧光染色法和TUNEL分析法观察恩度诱导MCF-7细胞凋亡的形态变化,蛋白印迹法检测恩度作用的MCF-7细胞中与生长和凋亡相关蛋白的表达.结果表明,恩度显著性地抑制MCF-7细胞的生长并诱导细胞凋亡.此外,恩度显著性地减少MCF-7细胞VEGFR1,c-Met,ERα,Akt,NF-κB,Bcl-2和CyclinD1蛋白的表达,明显地上调Bax蛋白的表达,其作用的分子机制可能是通过抑制VEGFR1/c-Met/ERα-Akt-NF-κB信号传导通路,下调Bcl-2/Bax蛋白比率、降低CyclinD1蛋白的水平.
The effects of recombinant human endostatin Endostar on cell growth of estrogen receptor-positive human breast cancer MCF-7 cell line and the molecular mechanisms of action are investigated. The growth inhibition of MCF-7 cells by different concentrations of Endostar is evaluated using MTT, Trypan Blue staining and Neutral Red tests. The Endostar-induced apoptotic morphological changes in MCF-7 cells are detected using Hoechst 33258 stai- ning and TUNEL assay. The protein expressions related to the growth and apoptosis in MCF-7 cells treated with En- dostar are analyzed using Western blotting. The results show that Endostar significantly suppresses the growth of the MCF-7 cells and induces the apoptosis in MCF-7 cells. In addition, Endostor remarkably reduces the protein expressions of VEGFR1, c-Met, ERα, Akt, NF-κB, Bcl-2 and CyelinD1. It also markedly enhances the protein expressions of Bax in MCF-7 cells. The molecular mechanism of action may be related to the down-regulation of Bel- 2/Bax and Cyclin D1 protein expressions via inhibiting the signaling pathways of VEGFR1/c-Met/ERα-Akt-NF-κB in MCF-7 cells.
出处
《烟台大学学报(自然科学与工程版)》
CAS
2013年第2期123-130,共8页
Journal of Yantai University(Natural Science and Engineering Edition)
基金
国家科技部十二五"863"课题资助项目(2012AA020206)
国家自然科学基金资助项目(30973553/C180105)
山东省科技攻关项目(2009GG10002087)
山东省自然科学基金资助项目(ZR2012HM016)