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    
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.
Y Liu; M O Lee; H G Wang; Y Li; Y Hashimoto; M Klaus; J C Reed; X Zhang
Related Documents :
10595738 - Epidermal growth factor-dependent dissociation of crkii proto-oncogene product from the...
3266248 - Rheumatoid adherent synovial cells produce b cell differentiation factor activity neutr...
17457318 - Ras transformation mediates reovirus oncolysis by enhancing virus uncoating, particle i...
3876338 - Epidermal growth factor promotes the chemotactic migration of cultured rat intestinal e...
19487818 - The basics of epithelial-mesenchymal transition.
1255748 - Factors involved in concanavalin a agglutination of kb and nc37 cells grown in suspensi...
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    
La Jolla Cancer Research Foundation, Cancer Research Center, La Jolla, California 92037, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Apoptosis / drug effects*
Base Sequence
Breast Neoplasms / metabolism,  pathology*
Gene Transfer Techniques
Molecular Sequence Data
Receptors, Retinoic Acid / genetics,  metabolism*
Signal Transduction
Tretinoin / metabolism,  pharmacology*
Grant Support
Reg. No./Substance:
0/Receptors, Retinoic Acid; 0/retinoic acid receptor beta; 302-79-4/Tretinoin

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

Previous Document:  Cytoplasmic sequestration of wild-type p53 protein impairs the G1 checkpoint after DNA damage.
Next Document:  A highly amplified mouse gene is homologous to the human interferon-responsive Sp100 gene encoding a...