Autocrine IL-1β-TRAF6 signalling promotes squamous cell carcinoma invasion through paracrine TNFα signalling to carcinoma-associated fibroblasts

Oncogene. 2013 Feb 7;32(6):747-58. doi: 10.1038/onc.2012.91. Epub 2012 Mar 26.

Abstract

The invasion of squamous cell carcinoma (SCC) is a significant cause of morbidity and mortality. Here, we identify an E3 ligase, Traf6 and a de-ubiquitinating enzyme, Cezanne/ZA20D1, as important regulators of this process in organotypic models. Traf6 can promote the formation of Cdc42-dependent F-actin microspikes. Furthermore, Traf6 has a key role in autocrine interleukin-1β signalling in SCC cells, which in turn is required to drive the expression of tumour necrosis factor α (TNFα). TNFα acts in a paracrine manner to increase the invasion-promoting potential of carcinoma-associated fibroblasts (CAFs). Exogenous TNFα signalling can restore invasion in cells depleted of Traf6. In conclusion, Traf6 has two important roles in SCC invasion: it promotes cell intrinsic Cdc42-dependent regulation of the actin cytoskeleton and enables production of the paracrine signal, TNFα, that enhances the activity of CAFs.

MeSH terms

  • Autocrine Communication
  • Carcinoma, Squamous Cell / metabolism*
  • Endopeptidases / metabolism*
  • Fibroblasts / metabolism*
  • Humans
  • Interleukin-1beta / metabolism
  • Neoplasm Invasiveness
  • Paracrine Communication
  • Signal Transduction
  • TNF Receptor-Associated Factor 6 / metabolism*
  • Tumor Necrosis Factor-alpha / metabolism
  • cdc42 GTP-Binding Protein / metabolism

Substances

  • Interleukin-1beta
  • TNF Receptor-Associated Factor 6
  • Tumor Necrosis Factor-alpha
  • Endopeptidases
  • OTUD7B protein, human
  • cdc42 GTP-Binding Protein