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Gas6 protein promotes the progress of NSCLC cells through VEGFAKT pathway

机译:Gas6蛋白通过VEGFAKT途径促进NSCLC细胞的进展

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Purpose: To investigate the expression and mechanism of Gas6 in non-small cell lung cancer (NSCLC). Method: Western blot was performed to measure Gas6 expression in NSCLC tumor and adjacent tissues. Cultured NSCLC cell line A549 or normal epithelial cell HBE was treated with 100 or 200 ng/ml Gas6, and proliferation was measured by MTT assay. Caspase 3 activity was measured and cell invasion was described by Transwell assay. VEGF and AKT expression was detected by Western blot and the expression of interleukin-2 (IL-2) and IL-6 was assessed by ELISA. Results: Gas6 was significantly up-regulated in NSCLC tumor tissues compared to adjacent tissues (P<0.05). Treatment of A549 cells using Gas6 significantly facilitated tumor cell proliferation, decreased caspase 3 activity, facilitated tumor cell invasion, and enhanced VEGF protein level, pAKT, IL-2 and IL-6 expression (P<0.05) in a dose dependent manner. Conclusion: Gas6 is up-regulated in NSCLC tumor tissues and facilitates NSCLC cell proliferation or invasion, suppresses apoptosis to enhance NSCLC tumor progression probably via modulating VEGF/AKT signal.
机译:目的:探讨Gas6在非小细胞肺癌(NSCLC)中的表达和机制。方法:进行蛋白质印迹以测量NSCLC肿瘤和相邻组织中的Gas6表达。培养的NSCLC细胞系A549或普通上皮细胞HBE被100或200ng / mL气体6处理,并通过MTT测定法测量增殖。测定胱天蛋白酶3活性,并通过Transwell测定描述细胞侵蚀。通过蛋白质印迹检测VEGF和AKT表达,ELISA评估白细胞介素-2(IL-2)和IL-6的表达。结果:与相邻组织相比,Gas6在NSCLC肿瘤组织中显着上调(P <0.05)。使用Gas6治疗A549细胞显着促进肿瘤细胞增殖,降低Caspase 3活性,促进的肿瘤细胞侵袭和增强型VEGF蛋白水平,PAKT,IL-2和IL-6表达(P <0.05)。结论:Gas6在NSCLC肿瘤组织中上调,促进NSCLC细胞增殖或侵袭,抑制细胞凋亡,可能通过调节VEGF / AKT信号来增强NSCLC肿瘤进展。

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