摘要
目的:检测TGFβ1、TGFβ受体Ⅱ及其下游Smad调节因子等基因在乳腺癌和正常乳腺上皮细胞中的表达,探讨TGFβ在乳腺癌发展过程中发挥作用的分子机制。方法:分离纯化人正常乳腺上皮细胞,应用RT-PCR检测乳腺癌细胞系MCF7及正常乳腺上皮细胞中TGFβ1、TGFβ受体Ⅱ、Smad4、Smad6、Smad7的表达。结果:TGFβ1、TGFβ受体Ⅱ、Smad6、Smad7与内参照GAPDH比值在正常乳腺上皮细胞中(0.721±0.214、1.001±0.312、0.689±0.12和0.221±0.124)与MCF7细胞(0.698±0.324、0.998±0.217、0.718±0.257;0.246±0.138)比较表达水平差异无显著性,Smad4在乳腺癌细胞中的表达水平(0.498±0.221)低于正常乳腺上皮细胞(1.132±0.314)(P<0.05)。结论:Smad4在乳腺癌细胞中的低表达可能与TGFβ对乳腺癌的促癌作用有关联。
Objective To explore the molecular mechanism of TGFβ in the progress of breast cancer by examining the expressions of TGFβ1 , TGFβ receptor Ⅱ and Smad transcriptional factors in normal human breast epithelium cells and MCF7 cells. Methods RT-PCR was used to measure the expression levels of TGFβ1 , TGFβ receptor Ⅱ , Smad4, Smad6 and Smad7 in normal human breast epithelium cells and MCF7 cells. Results There were no any significant differences of the ratios of TGFβ1, TGFβ receptorⅡ, Smad6, Smad7 to GAPDH between normal human breast epithelium cells (0. 721 ± 0. 214, 1. 001 ± 0. 312, 0. 689 ± 0.12, 0. 221 ± 0. 124) and MCF7 cells (0. 698±0. 324, 0. 998±0. 217, 0. 718±0. 257, 0. 246±0. 138) while the expression of Smad4 in MCF7 cells was significantly lower than that in normal human breast epithelium cells (P〈0. 05). Conclusion The low expression of Smad4 in MCF7 cells may be associated with the promotion effect of TGFβ on breast cancer.
出处
《吉林大学学报(医学版)》
CAS
CSCD
北大核心
2009年第1期142-145,共4页
Journal of Jilin University:Medicine Edition
基金
国家863重大专项基金资助课题(2004AA205020)
教育部博士学科点专项科研基金资助课题(20020183064)