Document Detail


Effects of novel retinoic acid metabolism blocking agent (VN/14-1) on letrozole-insensitive breast cancer cells.
MedLine Citation:
PMID:  17145897     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Aromatase inhibitors are proving to be more effective than tamoxifen for postmenopausal estrogen receptor (ER)-positive breast cancer. However, the inevitable development of resistance to treatment is a concern. We investigated the effects of novel retinoic acid metabolism blocking agent, VN/14-1, in overcoming letrozole resistance in long-term letrozole cultured (LTLC) cells. Compared with MCF-7 cells stably transfected with aromatase (MCF-7Ca), LTLC cells were no longer sensitive to growth inhibition by aromatase inhibitors. The HER-2/phosphorylated mitogen-activated protein kinase (pMAPK) growth factor signaling pathways were activated, and ERalpha and coactivator amplified in breast cancer 1 (AIB1) were up-regulated approximately 3-fold in LTLC cells. VN/14-1 inhibited aromatase activity and growth values of in MCF-7Ca cells with IC(50) of 8.5 and 10.5 nmol/L, respectively. In human placental microsomes, aromatase activity was inhibited with IC(50) of 8.0 pmol/L. The IC(50) in LTLC cells was 0.83 nmol/L, similar to letrozole (IC(50), 0.3 nmol/L) in MCF-7Ca cells. LTLC cells were 10-fold more sensitive to growth inhibition by VN/14-1 than MCF-7Ca cells. VN/14-1 treatment effectively down-regulated ERalpha, AIB1, pMAPK, HER-2, cyclin D1, cyclin-dependent kinase 4 (CDK4), and Bcl2 and up-regulated cytokeratins 8/18, Bad, and Bax. Tumor growth of LTLC cells in ovariectomized nude mice was independent of estrogens but was inhibited by VN/14-1 (20 mg/kg/d; P < 0.002). Decreases in ERalpha, cyclin D1, CDK4, and pMAPK and up-regulation of cytokeratins, Bad, and Bax with VN/14-1 in tumor samples may be responsible for the efficacy of this compound in inhibiting LTLC cell growth in vitro and in vivo.
Authors:
Aashvini Belosay; Angela M H Brodie; Vincent C O Njar
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Cancer research     Volume:  66     ISSN:  0008-5472     ISO Abbreviation:  Cancer Res.     Publication Date:  2006 Dec 
Date Detail:
Created Date:  2006-12-05     Completed Date:  2007-01-10     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  11485-93     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Experimental Therapeutics, School of Medicine and the Greenebaum Cancer Center, University of Maryland, Baltimore, Maryland 21201, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis Regulatory Proteins / metabolism
Aromatase / metabolism
Aromatase Inhibitors / pharmacology
Blotting, Western
Breast Neoplasms / drug therapy,  metabolism*,  pathology
Cell Cycle Proteins / metabolism
Cell Line, Tumor
Cell Proliferation / drug effects
Dose-Response Relationship, Drug
Drug Resistance, Neoplasm / drug effects
Estrogen Receptor alpha / metabolism
Female
Histone Acetyltransferases / metabolism
Hormones / pharmacology
Humans
Imidazoles / pharmacology*
Mice
Mice, Nude
Microsomes / drug effects,  enzymology
Mitogen-Activated Protein Kinases / metabolism
Nitriles / pharmacology*
Nuclear Receptor Coactivator 3
Ovariectomy
Placenta / enzymology
Pregnancy
Trans-Activators / metabolism
Tretinoin / analogs & derivatives*,  antagonists & inhibitors,  metabolism*,  pharmacology
Triazoles / pharmacology*
Xenograft Model Antitumor Assays
Grant Support
ID/Acronym/Agency:
CA-62483/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/4-(1H-imidazol-1-yl)retinoic acid; 0/Apoptosis Regulatory Proteins; 0/Aromatase Inhibitors; 0/Cell Cycle Proteins; 0/Estrogen Receptor alpha; 0/Hormones; 0/Imidazoles; 0/Nitriles; 0/Trans-Activators; 0/Triazoles; 112809-51-5/letrozole; 302-79-4/Tretinoin; EC 1.14.14.1/Aromatase; EC 2.3.1.48/Histone Acetyltransferases; EC 2.3.1.48/NCOA3 protein, human; EC 2.3.1.48/Ncoa3 protein, mouse; EC 2.3.1.48/Nuclear Receptor Coactivator 3; EC 2.7.11.24/Mitogen-Activated Protein Kinases

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


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