SATB1基因与MDR1基因在大肠癌细胞中的相关性研究

The SATB1 gene and MDR1 gene in the multidrug resistance of colorectal cancer cells： a correlation study

目的探讨特异AT序列结合蛋白1（special AT-rich sequence—bindingprotein1，SATB1）基因表达对大肠癌细胞SW620内多药耐药基因（muhidrugresistancegene，MDR1）表达的影响，并初步探讨SATB1基因参与大肠癌多药耐药的机制。方法将3对靶向针对SATB1基因的小片段干扰核糖核酸（smallinterferingRNA，siR-NA）与脂质体转染复合物转染至SW620细胞，采用Westernblot分别检测SATB1蛋白和P-糖蛋白（P-glycopro-tein，P-gP）的表达，CCK8法检测基因转染前后SW620细胞对化疗药物5-氟尿嘧啶（5-fluouracil，5-Fu）、长春新碱的敏感性。结果Westernblot显示转染后SW620细胞内SATB1蛋白表达显著降低（P〈0．05），而P-gp的表达水平亦显著降低（P〈0．05）；CCK8法检测结果显示SATB1基因转染后SW620细胞增强了对5-Fu、长春新碱的敏感性（P〈0．05）。结论下调SATB1基因可以下调SW620细胞中MDR1基因的表达，逆转SW620细胞的多药耐药。

Objective To investigate the effects of special AT - rich sequence - binding protein 1 （ SATB1 ） gene on the expression of muhidrug resistance 1 （ MDR1 ） gene in colorectal cancer cell line SW620, and to explore the mech- anism by which SATB1 gene involves in the MDR of colorectal cancer. Methods The specific sequences of SATB1 small interfering RNA （siRNA） were designed and synthesized in vitro, then transfected into SW620 cells using lipo- fectamine 2000 reagent. The levels of SATB1 and P - gp were examined by Western blot. The cellular sensitivity to che- motherapeutic treatment was detected by CCK8 method. Results According to western blot, the expression of SATB1 in SW620 was significantly decreased （P 〈 0.05 ）, in contrast with a reduced level of P - gp （ P 〈 0.05 ）. Meanwhile, CCK8 method indicated that SW620 cells enhanced their cellular sensitivity to chemotherapeutic treatment after SATB1 gene was silenced （P 〈 0.05 ）. Conclusion Down - regulation of SATB1 by siRNA could reduce the expression of MDR1 gene in SW620 ceils so as to reverse the MDR of the ceils.