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Effect of PI3K gene silencing on growth, migration and related proteins expression of CD40 signal-mediated gastric cancer cells

机译:PI3K基因沉默对CD40信号介导的胃癌细胞生长,迁移及相关蛋白表达的影响

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In this study, we investigate effect of PI3K gene silencing on growth, migration and related proteins expression of CD40 signal-mediated gastric cancer cells. We observed that combination of sCD40L with PI3K siRNA could significantly inhibit AGS cellsgrowth, block cells in G1 phase, and promote tumour cells apoptosis after 24 h treatment. Transwell test showed that numbers of cells per visual field in group PI3K siRNA or group sCD40L (after 24 h PI3K siRNA or sCD40L alone treatment) were fewer thanthat (32.54 ± 4.22) in control group. Numbers of cells per visual field in (after 24 h combination treatment of PI3K siRNA with sCD40L) were significantly fewer than that in group PI3K siRNA or group sCD40L. Compared with group sCD40L, expression levelof Fas protein in group sCD40L + PI3K siRNA was significantly increased. The findings suggest that PI3K siRNA may strengthen CD40-induced specific antitumour effect via blocking PI3K/Akt signal pathway, resisting tumour immunoediting regulated by CD40 signal. Combination of sCD40L and PI3K siRNA is an important mechanism of gastric cancer therapy.
机译:在这项研究中,我们调查了PI3K基因沉默对CD40信号介导的胃癌细胞生长,迁移和相关蛋白表达的影响。我们观察到,sCD40L与PI3K siRNA的结合可显着抑制AGS细胞的生长,阻断G1期的细胞,并促进24 h治疗后肿瘤细胞的凋亡。 Transwell试验表明,PI3K siRNA组或sCD40L组(单独使用PI3K siRNA或sCD40L处理24小时后)每视野的细胞数少于对照组(32.54±4.22)。 (PI3K siRNA与sCD40L联合处理24小时后)每个视野的细胞数明显少于PI3K siRNA组或sCD40L组。与sCD40L组相比,sCD40L + PI3K siRNA组中Fas蛋白的表达水平明显升高。这些发现表明,PI3K siRNA可能通过阻断PI3K / Akt信号通路来增强CD40诱导的特异性抗肿瘤作用,抵抗CD40信号调节的肿瘤免疫编辑。 sCD40L和PI3K siRNA的组合是胃癌治疗的重要机制。

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