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作 者:肖鹏[1] 初明[1] 孙泽文[1] 杜毅聪[1] 张明波[2] 徐兰[1] 初正云[2] 陈雪[1] 何嘉勰[1] 丁玲昱 焦运燊 王月丹[1]
机构地区:[1]北京大学医学部基础医学院,北京100191 [2]辽宁中医药大学药学院,辽宁沈阳110032
出 处:《现代生物医学进展》2015年第1期1-3,8,共4页Progress in Modern Biomedicine
基 金:国家自然科学基金项目(81172884);国家基础科学人才培养基金(J1030831/J0108);北京大学创新人才培养计划;北京大学医学部新教师启动基金项目(BMU0239)
摘 要:目的:本研究探讨了癌睾丸抗原TFDP3与乳腺癌细胞上皮间质化(epithelial-mesenchymal transition,EMT)的关系。方法:本研究中选取了乳腺癌细胞系(MCF-10A,MCF-7,SK-BR-3和MDA-MB-231)作为研究对象,通过Western Blot的方法筛选获得了TFDP3低水平表达的乳腺癌细胞株。进一步通过质粒转染的方式构建TFDP3过表达的细胞系模型,观察TFDP3在EMT中的作用。结果:TFDP3在MCF-10A及SK-BR-3中不表达,在间质化程度较高的MDA-MB-231中高水平表达,而在上皮化程度较高的MCF-7中的低水平表达。MCF-7中过表达TFDP3后,上皮细胞标记分子E-cadherin表达下调,而间质细胞标记分子N-cadherin、Snail、Twist及细胞骨架蛋白Vimentin表达上调。结论:TFDP3可以促进乳腺癌细胞发生EMT。Objective: To study the relationship between cancer testis antigen TFDP3 and epithelial- mesenchymal transition(EMT) in breast cancer. Methods: In this study, the breast cancer cell lines(MCF-10 A, MCF-7, SK-BR-3 and MDA-MB-231) were analyzed by Western Blot to obtain a TFDP3 positive strain with lower expression. Then, we established a TFDP3 over-expression cell line by plasmid transfection, and observed the role of TFDP3 in EMT. Results: TFDP3 was not detected in MCF-10 A and SK-BR-3, but at a relatively high level in MDA-MB-231 which exhibited as a mesenchymal cell line, and at a low level in MCF-7 which retains epithelial characteristics. Once MCF-7 over-expressed TFDP3, the epithelial cell marker E-cadherin was down-regulated, and the mesenchymal cell markers were up-regulated, including N-cadherin, Snail, Twist and cytoskeletal proteins Vimentin. Conclusion: TFDP3 might play an important role in promoting EMT in breast cancer cells.
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