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作 者:吴坚[1] 丁亚琴[1] 邵筱宏 竺春玲 谢心[1]
机构地区:[1]上海市中西医结合医院内分泌科,上海200082
出 处:《中国临床医学》2013年第6期759-761,共3页Chinese Journal of Clinical Medicine
基 金:上海市虹口区卫生局基金(编号:1103-07)
摘 要: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。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.
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