|
|
||||||||
J. Biol. Chem., Vol. 275, Issue 22, 16497-16505, June 2, 2000
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
From the Departments of ¶ Molecular Biology, Université
de Montréal, § Division of Experimental Medicine,
McGill University, and the Retinoids are essential for normal
epidermal growth and differentiation and show potential for the
prevention or treatment of various epithelial neoplasms. The retinoic
acid receptors (RAR
Characterization of Retinoic Acid Receptor-deficient
Keratinocytes*
,
§,
,
, and
§¶
Institut de Recherches
Cliniques de Montréal, 110 Avenue des Pins, Ouest,
Montréal, Québec H2W 1R7, Canada
, -
, and -
) are transducers of the retinoid
signal. The epidermis expresses RAR
and RAR
, both of which are
potential mediators of the effects of retinoids in the epidermis. To
further investigate the role(s) of these receptors, we derived
transformed keratinocyte lines from wild-type, RAR
, RAR
, and
RAR
null mice and investigated their response to retinoids,
including growth inhibition, markers of growth and differentiation, and
AP-1 activity. Our results indicate that RAR
is the principle
receptor contributing to all-trans-retinoic acid
(RA)-mediated growth arrest in this system. This effect partially correlated with inhibition of AP-1 activity. In the absence of RARs,
the synthetic retinoid N-(4-hydroxyphenyl)-retinamide
inhibited growth; this was not observed with RA, 9-cis RA,
or the synthetic retinoid (E)-4-[2-(5, 5, 8, 8 tetramethyl-5,6,7,8-tetrahydro-2-naphthalenyl)-1-propenyl] benzoic
acid. Finally, both RAR
and RAR
differently affected the
expression of some genes, suggesting both specific and overlapping roles for the RARs in keratinocytes.
*
This work was supported by the National Cancer Institute of
Canada with funds from the Canadian Cancer Society (to D. L.) and
by personnel support from the Medical Research Council of Canada (to
P. G.), the Cancer Research Society, Inc. (to C. F. C.),
and the Fonds de la Recherches en Santé de Québec (to
D. L.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Inst. de
Recherches Cliniques de Montréal, 110 Ave. des Pins, Ouest,
Montréal, Québec H2W 1R7, Canada. Fax: 514-987-5767;
E-mail: lohnesd@ircm.qc.ca.
This article has been cited by other articles:
![]() |
R. F. Gillespie and L. J. Gudas Retinoic Acid Receptor Isotype Specificity in F9 Teratocarcinoma Stem Cells Results from the Differential Recruitment of Coregulators to Retinoic Acid Response Elements J. Biol. Chem., November 16, 2007; 282(46): 33421 - 33434. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Mar and P. A. Hoodless Embryonic fibroblasts from mice lacking tgif were defective in cell cycling. Mol. Cell. Biol., June 1, 2006; 26(11): 4302 - 4310. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Szanto and L. Nagy Retinoids Potentiate Peroxisome Proliferator-Activated Receptor {gamma} Action in Differentiation, Gene Expression, and Lipid Metabolic Processes in Developing Myeloid Cells Mol. Pharmacol., June 1, 2005; 67(6): 1935 - 1943. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. F. Chen and D. Lohnes Dominant-negative Retinoic Acid Receptors Elicit Epidermal Defects through a Non-canonical Pathway J. Biol. Chem., January 28, 2005; 280(4): 3012 - 3021. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. L. Crowe, R. Kim, and R. A.S. Chandraratna Retinoic Acid Differentially Regulates Cancer Cell Proliferation via Dose-Dependent Modulation of the Mitogen-Activated Protein Kinase Pathway Mol. Cancer Res., May 1, 2003; 1(7): 532 - 540. [Abstract] [Full Text] [PDF] |
||||
![]() |
Q. Xu, T. Konta, A. Furusu, K. Nakayama, J. Lucio-Cazana, L. G. Fine, and M. Kitamura Transcriptional Induction of Mitogen-activated Protein Kinase Phosphatase 1 by Retinoids. SELECTIVE ROLES OF NUCLEAR RECEPTORS AND CONTRIBUTION TO THE ANTIAPOPTOTIC EFFECT J. Biol. Chem., October 25, 2002; 277(44): 41693 - 41700. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Kawabata, K.-i. Kawahara, T. Kanekura, N. Araya, H. Daitoku, M. Hatta, N. Miura, A. Fukamizu, T. Kanzaki, I. Maruyama, et al. Possible Role of Transcriptional Coactivator P/CAF and Nuclear Acetylation in Calcium-induced Keratinocyte Differentiation J. Biol. Chem., March 1, 2002; 277(10): 8099 - 8105. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Hatoum, M. E. El-Sabban, J. Khoury, S. H. Yuspa, and N. Darwiche Overexpression of retinoic acid receptors alpha and gamma into neoplastic epidermal cells causes retinoic acid-induced growth arrest and apoptosis Carcinogenesis, December 1, 2001; 22(12): 1955 - 1963. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Goyette, D. Allan, P. Peschard, C. F. Chen, W. Wang, and D. Lohnes Regulation of Gli Activity by All-trans Retinoic Acid in Mouse Keratinocytes Cancer Res., October 1, 2000; 60(19): 5386 - 5389. [Abstract] [Full Text] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |