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The possible molecular regulation mechanism of CIK cells inhibiting the proliferation of Human Lung Adenocarcinoma NCL-H157 Cells

机译:CIK细胞抑制人肺腺癌NCL-H157细胞增殖的可能分子调控机制

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摘要

Cytokine-induced killer (CIK) cells were isolated and proliferation from human peripheral blood and cultured in appropriate growth medium. The biological characteristics of CIK cells were further determined by the characterization of surface markers by flow cytometry. CIK cells inhibited the proliferation of human lung adenocarcinoma NCL-H157 cells. Vascular endothelial growth factor (VEGF) expression was down-regulated in CIK cells co-cultured with NCL-H157 cells by western blotting analysis. Furthermore, in comparison with cells untreated by CIK, the NCL-H157 had a lower proliferation capacity. We proposed that the pharmacological mechanisms of NCL-H157 promoted by CIK can be estimated possibly with different biological significance that can be ascribed to down-regulated VEGF expression in vitro. The results suggest that the VEGF pathway guides developmental inhibiting of NCL-H157, and we speculate that the function of VEGF pathways is to guide NCL-H157 to inhibition by abundant CIK.
机译:分离细胞因子诱导的杀伤(CIK)细胞,并从人外周血中增殖,并在适当的生长培养基中培养。通过用流式细胞仪表征表面标志物进一步确定CIK细胞的生物学特性。 CIK细胞抑制人肺腺癌NCL-H157细胞的增殖。通过蛋白质印迹分析,在与NCL-H157细胞共培养的CIK细胞中,血管内皮生长因子(VEGF)的表达下调。此外,与未用CIK处理的细胞相比,NCL-H157具有较低的增殖能力。我们提出CIK促进NCL-H157的药理机制可能具有不同的生物学意义,可以归因于体外VEGF表达下调。结果表明,VEGF途径指导NCL-H157的发育抑制,我们推测VEGF途径的功能是指导NCL-H157抑制大量CIK。

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