Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Rapamycin potentiates cytotoxicity by docetaxel possibly through downregulation of Survivin in lung cancer cells | Niu et al. Journal of Experimental Clinical Cancer Research 2011 30 28 http content 30 1 28 Journal of Experimental Clinical Cancer Research RESEARCH Open Access Rapamycin potentiates cytotoxicity by docetaxel possibly through downregulation of Survivin in lung cancer cells Huiyan Niu Jiahe Wang Hui Li Ping He Abstract Background To elucidate whether rapamycin the inhibitor of mTOR mammalian target of rapamycin can potentiate the cytotoxic effect of docetaxel in lung cancer cells and to probe the mechanism underlying such enhancement. Methods Lung cancer cells were treated with docetaxel and rapamycin. The effect on the proliferation of lung cancer cells was evaluated using the MTT method and cell apoptosis was measured by flow cytometry. Protein expression and level of phosphorylation were assayed using Western Blot method. Results Co-treatment of rapamycin and docetaxel was found to favorably enhance the cytotoxic effect of docetaxel in four lung cancer cell lines. This tumoricidal boost is associated with a reduction in the expression and phosphorylation levels of Survivin and ERK1 2 respectively. Conclusion The combined application of mTOR inhibitor and docetaxel led to a greater degree of cancer cell killing than that by either compound used alone. Therefore this combination warrants further investigation in its suitability of serving as a novel therapeutic scheme for treating advanced and recurrent lung cancer patients. Background Despite recent advancement in the multidisciplinary treatment of cancer the prognosis for lung cancer remains poor in more advanced stages and recurrent cases. According to World Health Organization lung cancer ranks at the top in cancer-related mortalities in humans killing more than one million people each year. Mammalian target of rapamycin mTOR a serine threonine protein kinase of 289 kDa is critically involved in cellular signal transduction mediated by phosphatidylinositol 3 kinase PI3K 1 . The activation of mTOR
