Department of Pathology, The First Affiliated Hospital, Zhengzhou University, Zhengzhou, Henan 450052, PR China.
Oncol Rep. 2011 Feb;25(2):409-18. doi: 10.3892/or.2010.1078. Epub 2010 Dec 7.
It is well documented that B cell-specific Moloney murine leukemia virus integration site 1 (Bmi-1), widely overexpressed in the vast majority of malignancies, plays an essential role in the occurrence and development of several different tumors. Here, we report Bmi-1 siRNA-mediated cell proliferation inhibition and cell apoptosis in vitro and in vivo in the human breast carcinoma cell line MCF-7. Our results demonstrated that Bmi-1 siRNA effectively down-regulated the expression of Bmi-1, inhibited cell proliferation in vitro and in vivo, evoked cell cycle arrest in the G0/G1 phase and induced cell apoptosis in MCF-7 cells, coupled with decrease in cyclin D1, cyclin E, cdk2, bcl-2 and Ki-67 expression and Akt phosphorylation levels and an increase of p21 and bax expression and activities of caspase-3/-9. Taken together, our results suggest that Bmi-1 may be a potential molecular target for the therapy of breast carcinoma.
有大量文献记载，B 细胞特异性莫洛尼鼠白血病病毒整合位点 1（Bmi-1）在绝大多数恶性肿瘤中广泛过表达，在多种不同肿瘤的发生和发展中发挥着重要作用。在这里，我们报告了 Bmi-1 siRNA 介导的人乳腺癌细胞系 MCF-7 体外和体内的细胞增殖抑制和细胞凋亡。我们的结果表明，Bmi-1 siRNA 可有效下调 Bmi-1 的表达，抑制 MCF-7 细胞的体外和体内增殖，诱导细胞周期停滞在 G0/G1 期，并诱导细胞凋亡，同时降低细胞周期蛋白 D1、E、cdk2、bcl-2 和 Ki-67 的表达以及 Akt 磷酸化水平，增加 p21 和 bax 的表达以及 caspase-3/-9 的活性。综上所述，我们的研究结果表明，Bmi-1 可能是乳腺癌治疗的潜在分子靶点。
