Document Detail


Retinoic acid receptor beta mediates the growth-inhibitory effect of retinoic acid by promoting apoptosis in human breast cancer cells.
MedLine Citation:
PMID:  8622658     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Retinoids are known to inhibit the growth of hormone-dependent but not that of hormone-independent breast cancer cells. We investigated the involvement of retinoic acid (RA) receptors (RARs) in the differential growth-inhibitory effects of retinoids and the underlying mechanism. Our data demonstrate that induction of RAR beta by RA correlates with the growth-inhibitory effect of retinoids. The hormone-independent cells acquired RA sensitivity when the RAR beta expression vector was introduced and expressed in the cells. In addition, RA sensitivity of hormone-dependent cells was inhibited by a RAR beta-selective antagonist and the expression of RAR beta antisense RNA. Introduction of RAR alpha also restored RA sensitivity in hormone-independent cells, but this restoration was accomplished by the induction of endogenous RAR beta expression. Furthermore, we show that induction of apoptosis contributes to the growth-inhibitory effect of RAR beta. Thus, RAR beta can mediate retinoid action in breast cancer cells by promoting apoptosis. Loss of RAR beta, therefore, may contribute to the tumorigenicity of human mammary epithelial cells.
Authors:
Y Liu; M O Lee; H G Wang; Y Li; Y Hashimoto; M Klaus; J C Reed; X Zhang
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Molecular and cellular biology     Volume:  16     ISSN:  0270-7306     ISO Abbreviation:  Mol. Cell. Biol.     Publication Date:  1996 Mar 
Date Detail:
Created Date:  1996-06-18     Completed Date:  1996-06-18     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  8109087     Medline TA:  Mol Cell Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1138-49     Citation Subset:  IM    
Affiliation:
La Jolla Cancer Research Foundation, Cancer Research Center, La Jolla, California 92037, USA.
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects*
Base Sequence
Breast Neoplasms / metabolism,  pathology*
Female
Gene Transfer Techniques
Humans
Molecular Sequence Data
Receptors, Retinoic Acid / genetics,  metabolism*
Signal Transduction
Tretinoin / metabolism,  pharmacology*
Grant Support
ID/Acronym/Agency:
R01 CA60988/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Receptors, Retinoic Acid; 0/retinoic acid receptor beta; 302-79-4/Tretinoin
Comments/Corrections

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