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作 者:刘一诺[1] 刘阳[2] 江茜[1] 何苗[1] 韩丽[1] 颜媛媛[1] 魏敏杰[1]
机构地区:[1]中国医科大学药学院药理教研室,辽宁省分子靶向抗肿瘤药物药理学研究与评价重点实验室,辽宁沈阳110000 [2]沈阳医学院,辽宁沈阳110122
出 处:《现代肿瘤医学》2017年第11期1705-1708,共4页Journal of Modern Oncology
基 金:国家自然科学基金(编号:81572898,81501346);辽宁省高校创新团队计划资助项目(编号:LT2014016);辽宁省科技计划项目(编号:2014226033);沈阳市科技计划项目(编号:F16-094-1-00)
摘 要:目的:探究miR-100对乳腺癌细胞株MDA-MB-231迁移能力的调节与机制。方法:Real timePCR检测人正常乳腺上皮细胞MCF-10A和乳腺癌细胞株MDA-MB-231中miR-100的基础表达水平。应用脂质体法将miR-100 mimic及阴性对照分别转染乳腺癌细胞株MDA-MB-231,通过real time-PCR检测转染后miR-100的表达水平,细胞划痕实验检测过表达miR-100对MDA-MB-231细胞迁移能力的影响,Western blot方法检测slug、snail和E-cadherin等EMT蛋白表达水平的变化。结果:miR-100在乳腺癌细胞株MDA-MB-231中的表达明显低于人正常乳腺上皮细胞MCF-10A。转染miR-100 mimic的乳腺癌细胞株MDA-MB-231的miR-100表达水平明显增高,细胞划痕实验显示过表达miR-100的MDAMB-231细胞划痕愈合速度明显减慢。过表达miR-100的MDA-MB-231细胞E-cadherin蛋白表达水平明显增加,而slug和snail蛋白表达水平明显降低。结论:miR-100抑制乳腺癌细胞株MDA-MB-231的迁移能力与其上调E-cadherin,下调slug、snail蛋白表达,抑制EMT有关。ObjectiveTo investigate the effects and mechanisms of miR - 100 on the metastasis of breast cancer cell line MDA - MB -231. Methods: The expression of miR - 100 in human normal breast epithelial cells MCF - 10A and breast cancer cell line MDA - MB -231 were analyzed by real - time PCR. The expression of miR - 100 was detected by real time - PCR after transfecting miR -100 mimic or the negative control into MDA - MB - 231 breast cancer cell line. The cell migration ability of MDA - MB - 231 cells after transfection were detected by cell scratch test. The expression of slug,snail and E - cadherin were detected by Western blot. Results: The expression of miR - 100 in breast cancer cell line MDA - MB -231 was significantly lower than that in normal human breast epithelial cell line MCF - 10A. The expression of miR - 100 was significantly increased, cell scratches healing was significantly decreased, and the expression of E - cadherin protein was increased, while the expression of slug and snail protein was decreased in the MDA - MB -231 cells transfected with miR - 100 mimic. Conclusion:miR - 100 decreased the mi-gration ability of breast cancer cells by inhibiting the EMT of the cells.
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