IL-17 promoted metastasis of non-small-cell lung cancer cells

被引:107
|
作者
Li, Qinchuan [1 ]
Han, Yang [2 ]
Fei, Guangru [3 ]
Guo, Zhongliang [3 ]
Ren, Tao [3 ]
Liu, Zhongmin [1 ]
机构
[1] Tongji Univ, Sch Med, East Hosp, Dept Cardiothorac Surg, Shanghai 200120, Peoples R China
[2] Tongji Univ, Sch Med, East Hosp, Dept Pathol, Shanghai 200120, Peoples R China
[3] Tongji Univ, Sch Med, East Hosp, Dept Resp Med, Shanghai 200120, Peoples R China
基金
中国国家自然科学基金;
关键词
Lung cancer; NSCLC; Metastasis; IL-17; IL-6; TUMOR-GROWTH; INTERLEUKIN-17; BREAST; MICE; ANGIOGENESIS; AUTOIMMUNITY; FIBROSARCOMA; INFLAMMATION; EXPRESSION; RESPONSES;
D O I
10.1016/j.imlet.2012.10.011
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
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. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:144 / 150
页数:7
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