Interleukin-17 induces AP-1 activity and cellular transformation via upregulation of tumor progression locus 2 activity
Carcinogenesis, ISSN: 0143-3334, Vol: 34, Issue: 2, Page: 341-350
2013
- 37Citations
- 41Captures
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Metrics Details
- Citations37
- Citation Indexes37
- 37
- CrossRef31
- Captures41
- Readers41
- 41
Article Description
Inflammatory conditions elicited by extrinsic environmental factors promote malignant transformation, tumor growth and metastasis. Although the role of T cells in cancer promotion has been examined, little is known about the underlying molecular mechanisms of interleukin-17 A (IL-17A), a proinflammatory cytokine produced by activated CD4 memory T cells, in carcinogenesis. Here, we report that IL-17A induces neoplastic transformation of JB6 Cl41 cells through activation of tumor progression locus 2 (TPL2). IL-17A dose- and time-dependently increases TPL2 phosphorylation in JB6 Cl41 cells through IL-17A receptor. IL-17A activates mitogen-activated protein kinase/extracellular signal-regulated kinase kinases, c-jun N-terminal kinases and STAT3 signaling pathways, which are inhibited by a TPL2 kinase inhibitor (TKI). Furthermore, IL-17A activates c-fos and c-jun promoter activity, resulting in increased activator protein-1 (AP-1) activity. When small interfering RNA of IL-17A receptor (IL-17R), IL-17A and TPL2 were introduced into JB6 Cl41 cells, respectively, IL-17A-induced AP-1 activity was significantly decreased compared with control cells. Similarly, TPL2 inhibition suppressed AP-1 activity induced by IL-17A. The knockdown of IL-17R and TKI treatment in JB6 Cl41 cells resulted in decreased IL-17A-induced cell transformation. The in vivo chorioallantoic membrane assay also showed that IL-17A increased tumor formation of JB6 Cl41 cells, whereas TKI inhibited the tumorigenesis promoted by IL-17A. Consistent with these observations, knockdown of IL-17A and/or inhibition of TPL2 attenuated tumorigenicity of human breast cancer MCF7 cells. Together, our findings point to a critical role for the IL-17A-induced TPL2 signaling pathway in supporting cancer-associated inflammation in the tumor microenvironment. Therapeutic approaches that target this pathway may, therefore, effectively inhibit carcinogenesis. © The Author 2012. Published by Oxford University Press. All rights reserved.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84873529688&origin=inward; http://dx.doi.org/10.1093/carcin/bgs342; http://www.ncbi.nlm.nih.gov/pubmed/23125217; https://academic.oup.com/carcin/article-lookup/doi/10.1093/carcin/bgs342; https://dx.doi.org/10.1093/carcin/bgs342; https://academic.oup.com/carcin/article/34/2/341/2464074
Oxford University Press (OUP)
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