Abstract
Inflammation and angiogenesis are two hallmarks of carcinoma. The proinflammatory cytokine interleukin-17 (IL-17) facilitates angiogenesis in lung cancer; however, the underlying mechanism is not fully understood. In this study, tumour microvessel density (MVD) was positively associated with IL-17, interleukin-6 (IL-6), interleukin-8 (IL-8), and vascular endothelial cell growth factor (VEGF) expression in human lung adenocarcinoma tissues, and it was increased in tumour tissues of A549-IL-17 cell-bearing nude mice. Importantly, positive correlations were also detected between IL-17 expression and IL-6, IL-8 and VEGF expression in human lung adenocarcinoma tissues. Furthermore, IL-6, IL-8 and VEGF production, as well as STAT1 phosphorylation, were increased in tumour tissues of A549-IL-17 cell-bearing nude mice in vivo and in A549 and H292 cells following IL-17 stimulation in vitro. In addition, STAT1 knockdown using an inhibitor and siRNA attenuated the IL-17-mediated increases in IL-6, IL-8 and VEGF expression in A549 and H292 cells. In conclusion, IL-17 may promote the production of the angiogenic inducers IL-6, IL-8 and VEGF via STAT1 signalling in lung adenocarcinoma.
Highlights
Cancer is a leading cause of death in both more and less economically developed countries[1]
The relationship between IL-17, IL-6, IL-8, and vascular endothelial cell growth factor (VEGF) and microvessel density (MVD) determined by CD31 staining in human lung adenocarcinoma tissues was explored by Quantitative real-time PCR (qRT-PCR) and IHC
Our results revealed that MVD was positively associated with IL-17, IL-6, IL-8, and VEGF protein expression in human lung adenocarcinoma tissues (Fig. 1A–J and Fig. 2A,B)
Summary
Cancer is a leading cause of death in both more and less economically developed countries[1]. Angiogenesis is coordinated by several types of molecules[5], such as chemokines and cytokines Inflammation is another major hallmark of malignancy[4,5], including lung cancer[9,10]. IL-17 triggers tumour progression, mainly due to its proangiogenic properties by stimulating the production of angiogenic factors. Several reports have revealed that STAT3 is involved in IL-17-induced VEGF production in malignant tumours[18,19,20], including lung cancer[15], and one study[7] has demonstrated that IL-17 influences IL-6, IL-8 and VEGF expression in lung cancer cell lines via an unknown mechanism. Our results will provide a better understanding of the communication among IL-17, IL-6, IL-8, and VEGF as well as new insights into the targeting of inflammation and angiogenesis for the treatment of lung cancer
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