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miR-26a通过调控E2F7、Myc抑制乳腺癌MDA-MB-231细胞的增殖和迁移能力 被引量:4

The miR-26a inhibits proliferation and migration ability of MDA-MB-231 cells via regulation of E2F7 and Myc
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摘要 目的:研究miR-26a对乳腺癌MDA-MB-231细胞增殖和迁移能力的影响,并分析miR-26a调控增殖与迁移的可能机制。方法:应用实时荧光定量PCR法(QPCR)检测乳腺癌细胞系和正常乳腺上皮细胞中miR-26a的表达水平,并检测三阴型乳腺癌组织及相应正常乳腺组织中miR-26a与E2F7 mRNA的表达水平。应用脂质体介导的方法,以miR-26a mimics与E2F7 siRNA瞬时转染MDA-MB-231细胞,实时荧光定量PCR法检测miR-26a表达水平,Western blot法检测E2F7、Myc蛋白的表达水平。MTT法检测MDAMB-231细胞的增殖能力,划痕实验检测MDA-MB-231细胞迁移能力。结果:乳腺癌细胞中miR-26a的表达水平均低于正常乳腺细胞MCF-10A,且三阴型乳腺癌细胞表达水平降低最明显。三阴型乳腺癌组织中miR-26a相对于正常乳腺组织表达减低,而E2F7 mRNA表达则显著升高。miR-26a mimics转染后miR-26a表达水平显著升高,miR-26a过表达可抑制E2F7、Myc蛋白的表达;E2F7 siRNA转染后E2F7表达水平减低,Myc蛋白表达亦减低。MTT实验结果示miR-26a过表达可抑制MDA-MB-231细胞增殖,划痕实验示miR-26a过表达可抑制乳腺癌MDA-MB-231细胞迁移能力。结论:miR-26a可能通过抑制E2F7、Myc调控乳腺癌MDA-MB-231细胞的增殖与迁移能力。 Objective:To investigate the effect of miR -26a on proliferation and migration of breast cancer MDA -MB- 231 cells, then to explore its possible mechanism. Methods :The miR -26a and E2F7 expression of breast cancer cell lines, normal breast epithelial cell, triple negative breast cancer tissues and adjacent normal breast tissues were detected by using Real - time PCR (QPCR). Transient transfection of miR - 26a mimics and E2F7 siRNA to MDA -MB -231 cells were mediated by liposome. The miR -26a expression of MDA - MB -231 cell was detected by Real - time PCR,and the expression of E2F7 and Myc protein was detected by Western blot. The proliferation and migration ability were assessed by MTT and wound healing assay respectively. Results:The miR -26a levels of breast cancer cell lines were lower than that of normal breast cell MCF -10A,particularly triple negative breast cancer cell lines. Besides,the miR -26a expression of triple negative breast cancer tissues was inhibited compared to that of adja- cent normal breast tissues, while the E2F7 mRNA expression was elevated significantly. The miR -26a expression of MDA - MB -231 cell was elevated significantly after miR -26a mimics transfection. The overexpression of miR -26a decreased the expression of E2F7 and Myc protein, and the knockdown of E2F7 also decreased the expression of Myc. The miR -26a inhibited the proliferation and migration ability- of MDA - MB -231 cells according to MTT and wound healing assay- results. Conclusion: The miR -26a inhibited proliferation and migration ability- of MDA - MB -231 cells via possible mechanism of E2F7 and Myc repression.
作者 庞亚梅 王翠翠 李岁萍 宁谦 周博 任宏 Pang Yamei;Wang Cuicui;Li Suiping;Ning Qian;Zhou Bo;Ren Hong(Department of Respiratory and Critical Care Medicin;Department of Hematology and Endocrinology,Zoucheng People 's Hospital,Shandong Zoucheng 273500,China;Department of Thoracic Surgery and Oneology,the First Ajfiliated Hospital of Xign Jiaotong University,Shaanxi Xi Jan 710061,China.)
出处 《现代肿瘤医学》 CAS 2018年第13期1975-1979,共5页 Journal of Modern Oncology
基金 国家自然科学基金资助项目(编号:81272418) 陕西省自然科学基础研究计划(编号:2017JQ8059)
关键词 三阴型乳腺癌 miR-26a E2F7 MYC 增殖 迁移 triple negative breast cancer miR - 26a E2FT Myc proliferation migration
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