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Retinoid signaling in immortalized and carcinoma-derived human uroepithelial cells.

Authors
Waliszewski-P; Waliszewska-M; Gordon-N; Hurst-RE; Benbrook-DM; Dhar-A; Hemstreet-3rd-GP
Source
Mol Cell Endocrinol 1999 Feb; 148(1-2):55-65
NIOSHTIC No.
20031355
Abstract
This paper investigates the presence and functionality of retinoid signaling pathways in human urinary bladder carcinoma and SV40-immortalized uroepithelial cell lines. Only two of eight cell lines were proliferation-inhibited by 10 microM of either all-trans or 13-cis-retinoic acid. Transactivation of the CAT gene under control of a retinoid-responsive element demonstrated functionality of the signaling pathway in both sensitive cell lines and four of six resistant cell lines. Relative RT-PCR analysis of a panel of retinoid-responsive and inducible genes demonstrated changes in expression levels of all the genes in response to-retinoic acid treatment together with numerous aberrations dysregulations. We conclude that retinoid signaling may be a target for inactivation during tumorigenesis by uncoupling gene expression, proliferation and differentiation. Therefore retinoids are more likely to be effective for chemoprevention than for treatment of bladder carcinomas.
Keywords
Risk-factors; Risk-analysis; Cancer; Chemotherapy; Tumorigens; Tumorigenesis; Bladder-cancer; Biomarkers; Carcinogens; Carcinogenesis; Carcinogenicity; Exposure-assessment; Bladder-disorders; Urogenital-system-disorders
Contact
Department of Urology, University of Oklahoma Health Sciences Center, Oklahoma City 73190, USA
CODEN
MCEND6
Publication Date
19990201
Document Type
Journal Article
Email Address
robert-hurst@ouhsc.edu
Funding Amount
1994426
Funding Type
Grant
Fiscal Year
1999
NTIS Accession No.
NTIS Price
Identifying No.
Grant-Number-R01-OH-002647
Issue of Publication
1-2
ISSN
0303-7207
Source Name
Molecular and Cellular Endocrinology
State
OK
Performing Organization
University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
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