Document Detail


Identification of functionally distinct TRAF proinflammatory and phosphatidylinositol 3-kinase/mitogen-activated protein kinase/extracellular signal-regulated kinase kinase (PI3K/MEK) transforming activities emanating from RET/PTC fusion oncoprotein.
MedLine Citation:
PMID:  22158616     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Thyroid carcinomas that harbor RET/PTC oncogenes are well differentiated, relatively benign neoplasms compared with those expressing oncogenic RAS or BRAF mutations despite signaling through shared transforming pathways. A distinction, however, is that RET/PTCs induce immunostimulatory programs, suggesting that, in the case of this tumor type, the additional pro-inflammatory pathway reduces aggressiveness. Here, we demonstrate that pro-inflammatory programs are selectively activated by TRAF2 and TRAF6 association with RET/PTC oncoproteins. Eliminating this mechanism reduces pro-inflammatory cytokine production without decreasing transformation efficiency. Conversely, ablating MEK/ERK or PI3K/AKT signaling eliminates transformation but not pro-inflammatory cytokine secretion. Functional uncoupling of the two pathways demonstrates that intrinsic pro-inflammatory pathways are not required for cellular transformation and suggests a need for further investigation into the role inflammation plays in thyroid tumor progression.
Authors:
Josephine H F Wixted; Jay L Rothstein; Laurence C Eisenlohr
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-12-09
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  287     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-02-06     Completed Date:  2012-03-25     Revised Date:  2012-05-14    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3691-703     Citation Subset:  IM    
Affiliation:
Immunology and Microbial Pathogenesis Program, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Line, Tumor
Humans
Inflammation / genetics,  metabolism,  pathology
MAP Kinase Signaling System*
Mice
Mitogen-Activated Protein Kinase Kinases / genetics,  metabolism
NIH 3T3 Cells
Oncogene Proteins, Fusion / genetics,  metabolism*
Phosphatidylinositol 3-Kinases / genetics,  metabolism*
Protein-Tyrosine Kinases / genetics,  metabolism*
Rats
TNF Receptor-Associated Factor 2 / genetics,  metabolism*
TNF Receptor-Associated Factor 3 / genetics,  metabolism*
Thyroid Neoplasms / genetics,  metabolism*,  pathology
Grant Support
ID/Acronym/Agency:
F31 NS054444/NS/NINDS NIH HHS; F31NS054444/NS/NINDS NIH HHS; R01AI069192/AI/NIAID NIH HHS; R21A1063065//PHS HHS
Chemical
Reg. No./Substance:
0/Oncogene Proteins, Fusion; 0/TNF Receptor-Associated Factor 2; 0/TNF Receptor-Associated Factor 3; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC 2.7.1.112/RET-PTC oncoprotein, rat; EC 2.7.1.112/ret-PTC fusion oncoproteins, human; EC 2.7.10.1/Protein-Tyrosine Kinases; EC 2.7.12.2/Mitogen-Activated Protein Kinase Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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