Document Detail


Transcriptional regulation of pro-apoptotic Par-4 by NF-kappaB/p65 and its function in controlling cell kinetics during early events in endometrial tumourigenesis.
MedLine Citation:
PMID:  20186924     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Prostatic apoptosis response-4 (Par-4) was first identified in prostatic cancer cells that were induced to undergo apoptosis. Recently, Par-4 has been suggested to be a tumour suppressor gene that plays a role in the development of endometrial carcinomas (ECs), but the exact mechanism remains to be clarified. Here we examined gene activation signalling cascades and influence on cell kinetics during endometrial tumourigenesis. In normal endometrium, constitutively high levels of Par-4 expression were observed in epithelial cells through the menstrual cycle, in contrast to the transient up-regulation in stromal components in the menstrual stage, correlated positively with the phospho-p65 (pp65) status and apoptosis. In contrast, most ECs exhibited significant down-regulation as compared to normal endometrium, with positive links only to pp65 expression. In EC cell lines, transfection of the NF-kappaB subunit p65 led to transactivation of Par-4 through specific binding to its promoter region, in contrast to the suppression by active Akt, suggesting that the balance between the two signals may be important to determine Par-4 expression levels. In addition, transient overexpression of Par-4 resulted in the induction of not only apoptosis but also senescence, through changes in the expression of bcl-2 and p21$;{{\rm WAF1}}$, respectively. Together, these findings suggest that a signalling cascade involving sequential activation of NF-kappaB/p65 and Par-4 may participate in relatively early events of endometrial tumourigenesis, leading to modulation of cell kinetics including apoptosis and cell cycle progression.
Authors:
Makoto Saegusa; Miki Hashimura; Takeshi Kuwata; Isao Okayasu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of pathology     Volume:  221     ISSN:  1096-9896     ISO Abbreviation:  J. Pathol.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-04-08     Completed Date:  2010-05-11     Revised Date:  2011-02-07    
Medline Journal Info:
Nlm Unique ID:  0204634     Medline TA:  J Pathol     Country:  England    
Other Details:
Languages:  eng     Pagination:  26-36     Citation Subset:  IM    
Copyright Information:
Copyright (c) 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Affiliation:
Department of Pathology, Kitasato University School of Medicine, 1-15-1 Kitasato, Sagamihara, Kanagawa 228-8555, Japan. msaegusa@med.kitasato-u.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Adult
Aged
Aged, 80 and over
Apoptosis
Apoptosis Regulatory Proteins / metabolism*
Cell Aging
Cell Transformation, Neoplastic / metabolism*,  pathology
Endometrial Neoplasms / metabolism*,  pathology
Endometrium / metabolism
Female
Gene Expression Regulation, Neoplastic / physiology
Humans
Middle Aged
NF-kappa B / physiology*
Neoplasm Proteins / metabolism*
Reverse Transcriptase Polymerase Chain Reaction / methods
Transcription, Genetic
Tumor Cells, Cultured
Up-Regulation / physiology
Chemical
Reg. No./Substance:
0/Apoptosis Regulatory Proteins; 0/NF-kappa B; 0/Neoplasm Proteins; 0/prostate apoptosis response-4 protein

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