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Oncogenic activity of insulin in the development of non-small cell lung carcinoma

机译：胰岛素在非小细胞肺癌发展中的致癌活性

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Insulin is associated with the progression of numerous different types of cancer. However, the association between insulin and non-small cell lung carcinoma (NSCLC) remains unknown. The aim of the present study was to evaluate the role of insulin in the proliferation, migration and drug resistance of NSCLC cells, and to determine whether the phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathway was involved. NSCLC cells were treated with insulin in the absence or presence of , an inhibitor of the PI3K/Akt pathway. Following co-incubation with insulin, cell proliferation and drug resistance were measured by MTT; cell migration was examined by wound healing and Transwell assays; and the expression of cyclin A, proliferating cell nuclear antigen (PCNA), p27, matrix metalloproteinase 3 (MMP3), P-gp and proteins involved in the PI3K/Akt pathway were assessed via western blotting. The results of the current study demonstrated that insulin enhanced the proliferation, migration and drug resistance of NSCLC cells. Correspondingly, insulin upregulated the expression of cyclin A, PCNA, MMP3, P-gp and downregulated p27 expression in NSCLC cells. Following treatment with insulin, it was demonstrated that phospho-Akt expression increased in a dose-dependent manner. However, the effects of insulin on NSCLC cells was inhibited by the PI3K/Akt pathway inhibitor . Therefore, the results of the current study indicate that insulin is associated with the development of NSCLC by activating the PI3K/Akt pathway. This may improve understanding of the mechanism of action of insulin in NSCLC in the future.
机译：胰岛素与许多不同类型的癌症的进展有关。但是，胰岛素与非小细胞肺癌（NSCLC）之间的关联仍然未知。本研究的目的是评估胰岛素在非小细胞肺癌细胞增殖，迁移和耐药中的作用，并确定是否涉及磷酸肌醇3-激酶/蛋白激酶B（PI3K / Akt）途径。在存在或不存在PI3K / Akt途径抑制剂的情况下，用胰岛素处理NSCLC细胞。与胰岛素共孵育后，通过MTT测定细胞增殖和耐药性。通过伤口愈合和Transwell测定法检查细胞迁移； Western blot检测细胞周期蛋白A，增殖细胞核抗原（PCNA），p27，基质金属蛋白酶3（MMP3），P-gp和PI3K / Akt途径蛋白的表达。目前的研究结果表明，胰岛素增强了非小细胞肺癌细胞的增殖，迁移和耐药性。相应地，胰岛素在NSCLC细胞中上调细胞周期蛋白A，PCNA，MMP3，P-gp的表达，并下调p27的表达。用胰岛素治疗后，已证明磷酸化Akt表达以剂量依赖性方式增加。然而，PI3K / Akt途径抑制剂抑制了胰岛素对NSCLC细胞的作用。因此，本研究的结果表明，胰岛素通过激活PI3K / Akt途径与NSCLC的发展有关。将来可能会增进对胰岛素在非小细胞肺癌中作用机制的了解。

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