E-钙黏蛋白siRNA促进胃癌细胞SGC7901耐药与增殖

目的 研究E-钙黏蛋门siRNA对胃癌细胞SGC7901化疗敏感性和增殖能力的影响,并对其相关机制进行初步探讨.方法 用Lipofectamine 2000将E-钙黏蛋白siRNA及阴性对照序列转入细胞SGC7901,用MTT法检测细胞对药物的敏感性并观察细胞增殖能力.Western印迹法检测细胞E-钙黏蛋白、PTEN...

E-cadherin siRNA promotes drug resistance formation and proliferation in gastric cancer SGC7901 cell linein gastric cancer SGC7901 cell line

Objective: To explore the effect of E-cadherin siRNA on drug sensitivity and cell proliferation and their related mechanisms in SGC7901 cell line. Methods: SGC7901 cell line was transfected with E-cadherin siRNA by means of Lipofectamine 2000. Drug sensitivity of transfected cells to CDDP、5-FU、Paclitaxel and ADR was tested using MTT assay. And proliferation changes of cells were detected after transfection. Protein changes of E-cadherin, PTEN, AKT, p-AKT, Bax and Bcl-2 were detected by Western blot. Results: The E-cadherin protein expression was significantly decreased after E-cadherin siRNA transfection(P<0.05). The IC50 of CDDP、5-FU、Paclitaxel and ADR in E-cadherin siRNA tansfected group were significantly higher than in negative control group(4.375±0.199mg/L vs 2.882±0.166mg/L, 6.855±0.780mg/L vs 4.058±0.946mg/L, 2.530±0.259mg/L vs 1.483±0.225mg/L, 0.368±0.042mg/L vs 0.228±0.012mg/L respectively, P<0.05). Compared to the control group, cell proliferation was significantly increased in SGC7901 cell transfected with E-cadherin siRNA. The expression of PTEN and Bax protein were significantly lower than the control group 72h after trasfection(P<0.05), while the p-AKT and Bcl-2 protin was higher than the control group (P<0.05). Conclusion: E-cadherin siRNA can activate AKT pathway and regulate apoptotic balance, which may be one of mechanisms on promoting drug resistance and proliferation.