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

Immunol Lett. 2012 Dec 17;148(2):144-50. doi: 10.1016/j.imlet.2012.10.011. Epub 2012 Oct 23.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Carcinoma, Non-Small-Cell Lung / pathology*
  • Cell Line, Tumor
  • Cell Proliferation
  • Disease Progression
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Interleukin-17 / blood
  • Interleukin-17 / genetics
  • Interleukin-17 / metabolism*
  • Interleukin-6 / metabolism
  • Lung / metabolism
  • Lung / pathology
  • Lung Neoplasms / pathology*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Knockout
  • Mice, Nude
  • Neoplasm Metastasis
  • Neoplasm Staging
  • Receptors, Interleukin-17 / biosynthesis
  • Receptors, Interleukin-17 / metabolism
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction

Substances

  • Interleukin-17
  • Interleukin-6
  • Receptors, Interleukin-17
  • STAT3 Transcription Factor
  • Stat3 protein, mouse