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作 者:李丽春[1] 陈瑶[1] 付梅[1] 何谦[1] Li Lichun;Chen Yao;Fu Mei;He Qian(Outpatient Department,West China Hospital,Sichuan University,Chengdu,Sichuan,610041,China)
机构地区:[1]四川大学华西医院门诊
出 处:《西南国防医药》2019年第6期650-654,共5页Medical Journal of National Defending Forces in Southwest China
摘 要:目的观察沉默人乳腺癌MCF-7和MDA-MB-231细胞中钙结合蛋白S100A4基因对上皮间质转换(EMT)的影响。方法采用蛋白免疫印迹法(Western blot)和荧光实时定量(RT-PCR)检测S100A4在人乳腺癌组织中的表达情况。用RNA干扰技术将针对S100A4和非特异性阴性对照序列的siRNA转染至人乳腺癌MCF-7和MDA-MB-231细胞,采用RT-PCR和Western blot方法检测EMT相关分子(E-cadherin, N-cadherin、Snail和Slug)的表达在沉默组和对照组中的表达水平。结果成功建立S100A4基因沉默的人乳腺癌MCF-7和MAD-231细胞模型;二者细胞中N-cadherin、Snail和Slug表达水平降低,而Ecadherin表达水平上调。结论 S100A4通过调节EMT过程,促进乳腺癌的侵袭和迁移,其可能成为乳腺癌治疗新的靶标分子。Objective To observe the impact on epithelial-mesenchymal transition(EMT) by silencing S100 calcium-binding protein A4(S100 A4) in MCF-7 and MDA-MB-231 cells. Methods Western blot and RT-PCR were used to test the expression of S100 A4 in human breast cancer tissue. RNA interference was used to transfect the siRNA targeting S100 A4 and non-specific negative control sequence to MCF-7 and MDA-MB-231 cells, and then RT-PCR and Western blot were used to test the expression of EMTrelated molecules(E-cadherin, N-cadherin, Snail and Slug) in the silencing group and the control group. Results A cell model of MCF-7 and MAD-231 was successfully established on the basis that S100 A4 gene was silenced. The expression of N-cadherin, Snail and Slug in both cells was inhibited, while the expression of E-cadherin was up-regulated. Conclusion S100 A4 will promote the invasion and migration of breast cancer cells by adjusting EMT, making it a new possible target molecule to cure breast cancer.
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