molecular cross-talk between the nfκb and stat3 signaling pathways in head and neck squamous cell carcinoma

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ID: 190698
2006
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Abstract
The development of head and neck squamous cell carcinoma (HNSCC) involves the accumulation of genetic and epigenetic alterations in tumor-suppressor proteins, together with the persistent activation of growth-promoting signaling pathways. The activation of epidermal growth factor receptor (EGFR) is a frequent event in HNSCC. However, EGFR-independent mechanisms also contribute to the activation of key intracellular signaling routes, including signal transducer and activator of transcription-3 (STAT3), nuclear factor κB (NFκB), and Akt. Indeed, the autocrine activation of the gp130 cytokine receptor in HNSCC cells by tumor-released cytokines, such as IL-6, can result in the EGFR-independent activation of STAT3. In this study, we explored the nature of the molecular mechanism underlying enhanced IL-6 secretion in HNSCC cells. We found that HNSCC cells display an increased activity of the IL-6 promoter, which is dependent on the presence of an intact NFκB site. Furthermore, NFκB inhibition downregulated IL-6 gene and protein expression, and decreased the release of multiple cytokines. Interestingly, interfering with NFκB function also prevented the autocrine/paracrine activation of STAT3 in HNSCC cells. These findings demonstrate a cross-talk between the NFκB and the STAT3 signaling systems, and support the emerging notion that HNSCC results from the aberrant activity of a signaling network.
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squarize2006neoplasia:molecular Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Cristiane H. Squarize;Rogerio M. Castilho;Virote Sriuranpong;Decio S. Pinto, Jr.;Jorge Silvio Gutkind
Journal ACS chemical neuroscience
Year 2006
DOI
10.1593/neo.06274
URL
http://www.sciencedirect.com/science/article/pii/S1476558606800989
Keywords
cytokine oral cancer il-6 gene expression regulation Oncology including cancer and carcinogens tumors

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