کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3355604 | 1217193 | 2012 | 7 صفحه PDF | دانلود رایگان |

Non-small cell lung cancer (NSCLC) is the leading cause of cancer death worldwide. Recent data suggested that IL-17 might be a pivotal cytokine involved in tumor progression of NSCLC. However, the direct effect of IL-17 on metastasis of NSCLC cells still remains intractable. In this study, we found that the metastasis of NSCLC was significantly impaired in IL-17−/− mice. Further, we revealed that IL-17 could directly promote the invasion of NSCLC cells both in vitro and in vivo. Furthermore, we found that IL-6-Stat3 pathway was crucial for IL-17 to enhance the invasive potential of NSCLC cells. Finally, we found that elevated expression of IL-17 in peripheral blood was associated with the TNM stage, and elevated expression of IL-17R in NSCLC cells was associated with their invasive potential in NSCLC patients. These findings could facilitate our understanding of the potential role of IL-17 in tumor biology, and provide clues for developing promising strategies against NSCLC.
► The metastasis of NSCLC was significantly impaired in IL-17−/− mice.
► IL-17 directly promoted the invasion of NSCLC cells both in vitro and in vivo.
► Neutralization of IL-6 abrogated IL-17 enhanced metastasis of NSCLC.
► Elevated serological IL-17 was associated with TNM stages of NSCLC patients.
► Expression of IL-17R in NSCLC cells was correlated with their invasion.
Journal: Immunology Letters - Volume 148, Issue 2, 17 December 2012, Pages 144–150