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针对病种:乳腺癌

发表时间:2015年3月

发表国家:英国

登载刊物:食品与功能

研究单位:中国桂林,桂林医科大学部组织学和胚胎学学院

研究人员:陈俊,段玉鑫,张兴,等

主要结论:这些结果表明,金雀异黄素通过灭活IGF-1R-PI3 K / Akt通路并降低Bcl-2 / Bax mRNA和蛋白质的表达来抑制细胞增殖。 我们的发现有助于阐明金雀异黄素有助于预防乳腺癌癌变的可能机制.

Food & Function, 2015, 6(3):995-1000.

Genistein induces apoptosis by the inactivation of the IGF-1R/p-Akt signaling pathway in MCF-7 human breast cancer cells

Jun Chen, Yuxin Duan, Xing Zhang, et al

Department of Histology and Embryology, Guilin Medical University, Guilin, 541004, China

Genistein is an estrogenic soy-derived compound belonging to the isoflavone class and shows anti-cancer effects. However, the specific cell apoptosis mechanisms of genistein have not been fully understood. In this study, we investigated the specific cell apoptosis mechanisms of genistein and the potential involvement of the IGF1R-Akt-Bcl-2 and Bax-mediated pathways in human breast cancer cells in vitro. MCF-7 human breast cancer cells were treated with various concentrations of genistein, and cell proliferation was evaluated by the MTT assay. Morphological changes in treated cells were examined by Hoechst 33258 staining, and treated cells were examined by flow cytometry. The levels of IGF-1R, p-Akt, Bcl-2, and Bax protein expression and Bcl-2 and Bax mRNA expression were evaluated by western blot and RT-PCR, respectively. Genistein inhibited the proliferation of MCF-7 cells and induced cell apoptosis, as determined by Hoechst staining and flow cytometry analysis. Furthermore, genistein induced the inactivation of IGF-1R and p-Akt and downregulated the Bcl-2/Bax protein ratio. These results suggest that genistein inhibited cell proliferation by inactivating the IGF-1R-PI3 K/Akt pathway and decreasing the Bcl-2/Bax mRNA and protein expressions. Our findings help elucidate the mechanisms by which genistein may contribute to the prevention of breast cancer carcinogenesis.


英国《食品与功能》,
20153

MCF-7人体乳腺癌细胞中金雀异黄素通过IGF-1R/p-Akt信号通路的失活诱导细胞凋亡

陈俊,段玉鑫,张兴,等

中国桂林,桂林医科大学部组织学和胚胎学学院

金雀异黄素是一种大豆衍生的雌激素化合物,属于异黄酮类并表现出抗肿瘤作用。然而,金雀异黄素特异性的细胞凋亡机制还没有被完全了解。在本研究中,我们在体外人体乳腺癌细胞中探究了金雀异黄素以及IGF1R-Akt-Bcl-2Bax 介导通路可能参与的特异性细胞凋亡机制。用不同浓度的金雀异黄素治疗MCF-7 人体乳腺癌细胞,并用MTT检测法评价细胞增殖。处理后细胞的形态学变化由 赫斯特33258 染色,并且用流式细胞术检查治疗的细胞。通过蛋白质印迹和RT-PCR分别测试IGF-1Rp-AktBcl-2Bax蛋白的表达以及Bcl-2Bax mRNA的表达水平。通过Hoechst染色和流式细胞术分析测定,金雀异黄素可以抑制MCF-7细胞的增殖并诱导细胞凋亡。 此外,金雀异黄素诱导IGF-1Rp-Akt的失活,并下调Bcl-2 / Bax蛋白的比例。 这些结果表明,金雀异黄素通过灭活IGF-1R-PI3 K / Akt通路并降低Bcl-2 / Bax mRNA和蛋白质的表达来抑制细胞增殖。 我们的发现有助于阐明金雀异黄素有助于预防乳腺癌癌变的可能机制。
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