地特胰岛素对人乳腺癌细胞株MCF-7的增殖及凋亡的影响

目的：探讨地特胰岛素对人乳腺癌细胞株MCF-7的增殖和凋亡的影响及其分子机制.方法：用10 U/L地特胰岛素处理人乳腺癌细胞株MCF-7,处理不同时间后,用MTT法检测细胞的增殖情况,用流式细胞术检测细胞的凋亡情况,用Western blotting法检测胰岛素受体（insulin receptor,INS-R）和胰岛素样生长因子1类受体（type 1 insulin-like growth factor receptor,IGF-1R）的表达,用real-time PCR法检测B细胞淋巴瘤因子2（B cell lymphoma 2,Bcl 2）、IGF-1R、Myc-1和caspase-3的mRNA水平.结果：人乳腺癌细胞株MCF-7经地特胰岛素处理后,细胞增殖水平随处理时间的延长呈现增高趋势（r=0.753,P ＜0.01）,细胞凋亡水平则随处理时间的延长而降低（r=-0.821,P＜0.01）;INS-R和IGF-1R蛋白的表达水平随处理时间的延长而升高,之后有所降低;凋亡抑制基因Bcl-2、IGF-1R和Myc-1的mRNA水平也呈类似变化趋势（r=0.813,P＜0.01）,而促凋亡相关基因caspase-3则呈现相反的变化趋势（r=-0.719,P＜0.01）.结论：地特胰岛素处理可以促进人乳腺癌细胞株MCF-7的增殖并抑制其凋亡,其机制可能与促进凋亡抑制基因表达以及抑制凋亡基因表达有关.

Effects of Insulin Detemir on Proliferation and Apoptosis of Human Breast Cancer Cell Line MCF-7

Objective：To investigate the effects of insulin detemir on the proliferation and apoptosis of human breast cancer cell line MCF-7 and the underlying molecular mechanisms.Methods：Human breast cancer cell line MCF 7 was treated with 10 U/L insulin detemir.The proliferation and apoptosis was detected by MTT assay and flow cytometry,respectively.The protein expression levels of insulin receptor （INS-R） and type 1 insulin-like growth factor receptor （IGF-1R） were detected by Western blotting.The mRNA expression levels of B cell lymphoma 2 （Bcl-2）,IGF-1R,Myc-1 and caspase-3 were detected by RTPCR.Results：After being treated with insulin detemir,the proliferative level of MCF 7 was increased （r=0.753,P＜0.01）,while the apoptosis level was decreased （r=-0.821,P＜0.01） with the extension of processing time.The protein expression levels of INS-R and IGF-1R were increased and then decreased a little.The mRNA levels of apoptotic inhibitory genes,Bcl-2,IGF-1R and Myc-1 were increased （r=0.813,P＜0.01） while caspase-3 showed an opposite trend （r=-0.719,P＜0.01）.Conclusions：The insulin detemir treatment can promote the proliferation and inhibit the apoptosis of human breast cancer cell line MCF 7.The underlying mechanisms may be correlated with the up-regulations of apoptotic inhibitory genes and downregulations of pro-apoptotic genes.