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- 2016
CCL18与TGF-β促进乳腺癌EMT的比较
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Abstract:
摘要 目的:研究比较CCL18与β转化生长因子(TGF-β)促进乳腺癌细胞上皮间质化(EMT)的分子机制,从而进一步明确靶向CCL18和TGF-β所激活的信号通路,抑制乳腺癌浸润迁移的分子靶点.方法:设计并合成针对CCL18的受体基因PITPNM3的特异性siRNA,利用脂质体携带siRNA转染乳腺癌MCF-7细胞,沉默PITPNM3的表达,分别用CCL18和TGF-β处理乳腺癌细胞,用免疫荧光和western blot的方法检测EMT的特异性标志物E-cadherin和Vimentin表达的变化以及Smad2和Smad3的磷酸化状态.结果:PITPNM3-siRNA转染MCF-7细胞24 h后,用CCL18或TGF-β分别处理乳腺癌细胞4 d,western blot证明CCL18不能磷酸化激活Smad2和Smad3,TGF-β磷酸化激活Smad2和Smad3促进乳腺癌EMT,沉默PITPNM3表达,western blot和免疫荧光证明不影响TGF-β促进乳腺癌EMT.结论:TGF-β通过Smad2/smad3磷酸化激活促进乳腺癌EMT,不通过CCL18的受体PITPNM3发挥作用.
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