Document Detail


c-Jun promotes cellular survival by suppression of PTEN.
MedLine Citation:
PMID:  16676006     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Activation of c-Jun, a component of the AP-1 family of transcription factors, leads to either promotion or prevention of apoptosis. However, the molecular determinants of c-Jun-mediated cell survival are still unclear. We show here that inducible expression of c-Jun promotes cellular survival by negatively regulating the expression of the tumor-suppressor PTEN, resulting in the concomitant activation of the Akt survival pathway. Consistently, c-jun-/- fibroblasts, which are sensitive to nutrient deprivation, and human cell lines in which c-Jun expression is silenced, express elevated levels of PTEN. siRNA-mediated silencing of PTEN resulted in the reduction of cell-death owing to c-Jun deficiency. c-Jun was found to suppress PTEN expression by binding to a variant AP-1 site found in the 5' upstream sequences of PTEN promoter. Finally, an inverse correlation between c-Jun and PTEN levels was apparent in a panel of human tumor cell lines, independent of their p53 status. Together, the data demonstrate that c-Jun contributes to the promotion of cellular survival by regulating the expression of PTEN.
Authors:
K Hettinger; F Vikhanskaya; M K Poh; M K Lee; I de Belle; J-T Zhang; S A G Reddy; K Sabapathy
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-05-05
Journal Detail:
Title:  Cell death and differentiation     Volume:  14     ISSN:  1350-9047     ISO Abbreviation:  Cell Death Differ.     Publication Date:  2007 Feb 
Date Detail:
Created Date:  2007-01-15     Completed Date:  2007-03-16     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9437445     Medline TA:  Cell Death Differ     Country:  England    
Other Details:
Languages:  eng     Pagination:  218-29     Citation Subset:  IM    
Affiliation:
Laboratory of Molecular Carcinogenesis, Division of Cellular and Molecular Research, National Cancer Centre, 11, Hospital Drive, Singapore 169610, Singapore.
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MeSH Terms
Descriptor/Qualifier:
Animals
Base Sequence
Binding Sites
Cell Death
Cell Line, Tumor
Cell Survival
Enzyme Activation
Food Deprivation
Gene Expression Regulation, Neoplastic
Gene Silencing
Humans
Mice
Molecular Sequence Data
NIH 3T3 Cells
PTEN Phosphohydrolase / genetics,  metabolism*
Proto-Oncogene Proteins c-akt / metabolism
Proto-Oncogene Proteins c-jun / deficiency,  metabolism*
RNA, Messenger / genetics,  metabolism
RNA, Small Interfering / metabolism
Transcription Factor AP-1 / genetics
Chemical
Reg. No./Substance:
0/Proto-Oncogene Proteins c-jun; 0/RNA, Messenger; 0/RNA, Small Interfering; 0/Transcription Factor AP-1; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 3.1.3.48/PTEN protein, human; EC 3.1.3.48/Pten protein, mouse; EC 3.1.3.67/PTEN Phosphohydrolase

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


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