A novel IL-17 signaling pathway controlling keratinocyte proliferation and tumorigenesis via the TRAF4–ERK5 axis

Ling Wu(Cleveland Clinic), Xing Chen(Cleveland Clinic), Junjie Zhao(Cleveland Clinic), Bradley N. Martin(Cleveland Clinic), Jarod A. Zepp(Cleveland Clinic), Jennifer S. Ko(Cleveland Clinic), Chunfang Gu(Cleveland Clinic), Gang Cai(Shanghai Jiao Tong University), Wenjun Ouyang, Ganes C. Sen(Cleveland Clinic), George R. Stark(Cleveland Clinic), Bing Su(Shanghai Jiao Tong University), Charlotte M. Vines(The University of Texas at El Paso), Cathy Tournier(University of Manchester), Thomas A. Hamilton(Cleveland Clinic), Allison T. Vidimos(Cleveland Clinic), Brian Gastman(Cleveland Clinic), Caini Liu(Cleveland Clinic), Xiaoxia Li(Cleveland Clinic)
The Journal of Experimental Medicine
September 7, 2015
Cited by 226Open Access
Full Text

Abstract

Although IL-17 is emerging as an important cytokine in cancer promotion and progression, the underlining molecular mechanism remains unclear. Previous studies suggest that IL-17 (IL-17A) sustains a chronic inflammatory microenvironment that favors tumor formation. Here we report a novel IL-17-mediated cascade via the IL-17R-Act1-TRAF4-MEKK3-ERK5 positive circuit that directly stimulates keratinocyte proliferation and tumor formation. Although this axis dictates the expression of target genes Steap4 (a metalloreductase for cell metabolism and proliferation) and p63 (a transcription factor for epidermal stem cell proliferation), Steap4 is required for the IL-17-induced sustained expansion of p63(+) basal cells in the epidermis. P63 (a positive transcription factor for the Traf4 promoter) induces TRAF4 expression in keratinocytes. Thus, IL-17-induced Steap4-p63 expression forms a positive feedback loop through p63-mediated TRAF4 expression, driving IL-17-dependent sustained activation of the TRAF4-ERK5 axis for keratinocyte proliferation and tumor formation.


Related Papers

No related papers found

Powered by citation graph analysis