Interleukin-6 and insulin-like growth factor-1 synergistically promote the progression of NSCLC. (17th November 2018)

• Record Type: Journal Article
• Authors: Tang, Hexiao; Bai, Yuquan; Pan, Gaofeng; Wang, Xianguo; Wei, Yanhong; Yang, Zetian; Zhao, Jinping
• Is Part Of: Autoimmunity. Volume 51:Number 8(2018)
• Page Start: 399
• Page End: 407
• Publication Date: 2018-11-17
• Subjects: Non-small cell lung cancer -- Interleukin-6 -- insulin-like growth factor 1 -- signaling pathways -- tissue microarray-immunohistochemistry; Autoimmunity -- Periodicals; Autoimmune diseases -- Periodicals; 571.973
• DOI: 10.1080/08916934.2018.1550079
• Languages: English
• ISSNs: 0891-6934

Abstract

Abstract: The signaling pathways of interleukin-6 (IL-6) and insulin-like growth factor 1 (IGF-1) play an important role in the progression of lung cancer, and this study aimed to explore whether they can synergistically promote the progression of non-small cell lung cancer (NSCLC). We found that IL-6, glycoprotein 130 (GP130), IGF-1 and IGF-1R were highly expressed in NSCLC ( p = .000), and there was the correlation between GP130, IGF-1, and IGF-1R ( p < .01). The overall survival of patients with the co-expression of GP130 and IGF-1R was significantly shorter ( p = .0360). Co-stimulation of IL-6 and IGF-1 resulted in significantly enhanced in cell proliferation, ( p < .05), invasion ( p < .05), cycle ( p < .05), apoptosis ( p < .05), and the expression of signal molecules (GP130, IGF-1R, p-AKT, and p-ERK1/2) (all p < .05) in NSCLC cells. This experiment revealed that IL-6 and IGF-1 can synergistically promote the progression of NSCLC. The high expression of GP130 and IGF-1R is an independent risk factor for poor prognosis patients, and it is helpful to find a more accurate target for targeted therapy in NSCLC.