Document Detail


AP-1--The Jun proteins: Oncogenes or tumor suppressors in disguise?
MedLine Citation:
PMID:  20060892     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Since its discovery more than two decades ago the involvement of the Activating protein 1 (AP-1) in proliferation, inflammation, differentiation, apoptosis, cellular migration and wound healing has been intensively studied. A model based on the early studies suggested antagonistic roles for the Jun proteins in proliferation and transformation. c-Jun was suggested to enhance transformation whereas JunB suggested to inhibit it in an antagonistic manner. Surprisingly, despite accumulation of data obtained from animal models regarding the role of Jun proteins in cancer and identification of oncogenic pathways regulating them, their involvement in human cancer was not demonstrated until recently. Here, we will describe the current knowledge about the roles of Jun proteins in human neoplasia. We will focus on the pathological examples demonstrating that the initial dogma has to be reexamined. For example, like c-Jun, JunB seems to play an oncogenic role in lymphomas, particularly in Hodgkin's lympomas. Furthermore, unlike the antagonistic activities of c-Jun and JunB in the transcription of genes coding for major cell cycle regulators such as CyclinD or p16INK4A, the transcription of other cell cycle regulating genes is modified similarly by c-Jun or JunB. Interestingly, some of these genes such as the ones coding for CyclinA or p19(ARF) are important players in either positive or negative regulation of cellular proliferation and survival. Finally, we will also discuss results posing JNK, known so far as the major activator of c-Jun, as a negative regulator of c-Jun level and activity. These recent findings suggest that the role of each Jun protein in neoplasia as well as in cellular survival should be examined in a context-dependent manner.
Authors:
Eitan Shaulian
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2010-01-11
Journal Detail:
Title:  Cellular signalling     Volume:  22     ISSN:  1873-3913     ISO Abbreviation:  Cell. Signal.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-03-26     Completed Date:  2010-05-17     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8904683     Medline TA:  Cell Signal     Country:  England    
Other Details:
Languages:  eng     Pagination:  894-9     Citation Subset:  IM    
Copyright Information:
Copyright 2010 Elsevier Inc. All rights reserved.
Affiliation:
Department of Biochemistry and Molecular Biology, The Institute for Medical Research-Israel-Canada, The Hebrew University-Hadassah Medical School, Jerusalem, Israel. eitansh@ekmd.huji.ac.il
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MeSH Terms
Descriptor/Qualifier:
Cell Transformation, Neoplastic
Humans
JNK Mitogen-Activated Protein Kinases / metabolism
Neoplasms / etiology*,  genetics
Proto-Oncogene Proteins c-jun / metabolism,  physiology*
Transcription Factor AP-1 / metabolism
Tumor Suppressor Proteins / physiology*
Chemical
Reg. No./Substance:
0/Proto-Oncogene Proteins c-jun; 0/Transcription Factor AP-1; 0/Tumor Suppressor Proteins; EC 2.7.11.24/JNK Mitogen-Activated Protein Kinases

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