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目的:探讨同时抑制X连锁凋亡抑制蛋白(XIAP)和生存素(survivin)后,对胰腺癌Panc-1细胞上皮-间质转化(EMT)及侵袭性的影响,并初步探讨其机制。方法:在前期实验构建的胰腺癌Panc-1-XS细胞(XIAP和survivin同时稳定抑制)中,运用Transwell小室实验及划痕实验分别检测细胞侵袭和迁移能力;半定量Western印迹分别检测钙黏蛋白-E(E-cadherin,上皮标志物)、锌指转录因子(Slug)蛋白(间质标志物)及第10号染色体同源丢失性磷酸酶——张力蛋白基因(PTEN)和磷酸化蛋白激酶B(P-Akt)蛋白的表达情况。结果:Panc-1-XS细胞侵袭和迁移能力显著下降,同时伴随E-cadherin蛋白表达显著上调及Slug蛋白显著下调,即出现间质-上皮转化(MET);PTEN蛋白表达上调、P-Akt蛋白表达下调。结论:同时抑制XIAP和survivin表达,能部分逆转胰腺癌Panc-1细胞EMT表型,显著减弱其侵袭和迁移能力;此调控过程可能通过PTEN/PI3K/Akt途径实现。
OBJECTIVE: To investigate the effect of simultaneously inhibiting XIAP and survivin on the epithelial-mesenchymal transition (EMT) and invasiveness of pancreatic cancer Panc-1 cells and to explore its possible mechanism. Methods: The invasion and migration of Panc-1-XS cells (the simultaneous and stable inhibition of XIAP and survivin) in pancreatic cancer cells were detected by Transwell chamber assay and scratch assay. The expression of cadherin E-cadherin (epithelial marker), Slug protein (interstitial marker), and chromosome 10 homologous loss-type phosphatase-tensin gene (PTEN) and phosphorylated protein kinase B (P-Akt) protein expression. Results: The invasiveness and migration ability of Panc-1-XS cells were significantly decreased. Along with the significant up-regulation of E-cadherin protein expression and Slug protein downregulation, the expression of PTEN protein and P-Akt protein Down regulation. CONCLUSION: Simultaneous inhibition of XIAP and survivin expression can partially reverse the EMT phenotype of Panc-1 cells and significantly reduce the invasion and migration of pancreatic cancer Panc-1 cells. This regulation may be mediated through PTEN / PI3K / Akt pathway.