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作 者:胡嵩[1] 张岩巍[2] 姜鹏飞[3] 孙贝贝[1]
机构地区:[1]上海交通大学附属胸科医院中心实验室,上海200030 [2]上海交通大学附属胸科医院呼吸内科,上海200030 [3]上海市东方医院南院检验科,200123
出 处:《蚌埠医学院学报》2017年第1期27-29,33,共4页Journal of Bengbu Medical College
基 金:CSCO-先声抗肿瘤血管靶向治疗科研基金(Y-S 2014-003)
摘 要:目的:研究转录因子ETS-1通过调节miR-96对乳腺癌细胞增殖的影响。方法:通过RNAi技术下调乳腺癌细胞MCF-7中ETS-1的表达后,检测miR-96的表达;运用生物信息学方法预测转录因子ETS-1的结合位点,染色体免疫共沉淀反应加以验证;将miR-96转染入乳腺癌细胞MCF-7,观察对乳腺癌细胞增殖和克隆形成的影响。结果:抑制ETS-1表达,miR-96在乳腺癌细胞MCF-7中的表达明显上调(P<0.01);ETS-1通过结合在miR-96启动子区域,调节miR-96的表达;与对照组比较,过表达miR-96后,MCF-7的增殖能力和克隆形成能力均明显增强(P<0.01)。结论:ETS-1通过调节miR-96的表达,影响乳腺癌细胞增殖和克隆形成能力,有望在乳腺癌治疗中成为新的靶标。Objective: To investigate the effects of transcription factors ETS-1 on the proliferation of the breast cancer cells by regulating miR-96. Methods:The expression of miR-96 in breast cancer cell MCF-7 with silencing the ETS-1 expression induced by the RNA interference technique was detected. The binding site of transcription factor ETS-1 was predicted using bioinformatics method, and validated with chromatin immune precipitation reaction. The miR-96 was transfected into breast cancer cell MCF-7, and the effect of which on the proliferation and clone information of breast cancer cells was observed. Results : The expression of miR-96 in breast cancer cells was significantly increased after inhibiting the expression of ETS-1 (P 〈 0.01 ). The expression of ETS-1 was regulated by the ETS- 1 binding to the promoter region of miR-96. Compared with the control group, the abilities of proliferation and clone formation of MCF- 7 were significantly increased after the overexpression of miR-96 (P 〈 0.01 ). Conclusions:ETS-1 can affect the proliferation and clone formation ability of breast cancer ceils by regulating the expression of miR-96 ,which is expected to become a new target in the treatment of breast cancer.
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