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J Biol Chem, Vol. 273, Issue 41, 26915-26922, October 9, 1998

Overexpressed Activated Retinoid X Receptors Can Mediate Growth Inhibitory Effects of Retinoids in Human Carcinoma Cells

Haisu WanDagger , Marcia I. Dawson§, Waun K. Hong, and Reuben LotanDagger

From the Departments of Dagger  Tumor Biology and  Thoracic/Head and Neck Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030 and the § Retinoid Program, SRI International, Menlo Park, California 94025

Retinoic acid receptors (RARs) and retinoid X receptors (RXRs) mediate the effects of retinoids on gene expression by binding to response elements in retinoid-sensitive genes. RAR- but not RXR-selective retinoids were found in many previous studies to suppress the growth of various cells, implicating RXR-RAR in these effects. Using a co-expression vector for identifying cells that expressed retinoid receptors transiently and 5'-bromo-2'-deoxyuridine incorporation for labeling DNA-synthesizing cells, we found that RXR-selective retinoids inhibited DNA synthesis in squamous carcinoma 1483 cells transfected with RXRalpha but not with RARs. Ligand-induced transcription of the reporter luciferase gene via the activation of RXR-RXR but not RXR-RAR correlated with growth suppression. Studies with RXRalpha deletion mutants indicated that the DNA binding and the ligand binding domains are essential for mediating growth inhibition. A point mutation in the ligand binding domain (L430F) that decreased RXRalpha homodimerization compromised its growth inhibitory function. Further, RXRalpha mutant (F313A), which functions as a constitutively active receptor, inhibited DNA synthesis in the absence of ligand. These results demonstrate that RXR homodimer activation leads to growth inhibition and suggest that transfection of RXRalpha and treatment with RXR-selective retinoids or the transfection of constitutively activated RXRalpha mutant alone may have a therapeutic potential.

Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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