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Endocrine Reviews 26 (7): 898-915
Copyright © 2005 by The Endocrine Society

Interaction of Nuclear Receptors with the Wnt/ß-Catenin/Tcf Signaling Axis: Wnt You Like to Know?

David J. Mulholland, Shoukat Dedhar, Gerhard A. Coetzee and Colleen C. Nelson

Molecular and Medical Pharmacology (D.J.M.), University of California Los Angeles School of Medicine, Los Angeles, California 90095; The Prostate Centre at Vancouver General Hospital (D.J.M., S.D., C.C.N.), Vancouver, British Columbia, Canada V6H 3Z6; and University of Southern California/Norris Cancer Center, Keck School of Medicine (G.A.C.), Los Angeles, California 90033

Correspondence: Address all correspondence and requests for reprints to: David J. Mulholland, Department of Molecular and Medical Pharmacology, 650 Charles E. Young Drive, Center for Health Sciences 23-234, University of California Los Angeles School of Medicine, Los Angeles, California 90095. E-mail: dmulholland{at}mednet.ucla.edu

The cross-regulation of Wnt/ß-catenin/Tcf ligands, kinases, and transcription factors with members of the nuclear receptor (NR) family has emerged as a clinically and developmentally important area of endocrine cell biology. Interactions between these signaling pathways result in a diverse array of cellular effects including altered cellular adhesion, tissue morphogenesis, and oncogenesis. Analyses of NR interactions with canonical Wnt signaling reveal two broad themes: Wnt/ß-catenin modulation of NRs (theme I), and ligand-dependent NR inhibition of the Wnt/ß-catenin/Tcf cascade (theme II). ß-Catenin, a promiscuous Wnt signaling member, has been studied intensively in relation to the androgen receptor (AR). ß-Catenin acts as a coactivator of AR transcription and is also involved in cotrafficking, increasing cell proliferation, and prostate pathogenesis. T cell factor, a transcriptional mediator of ß-catenin and AR, engages in a dynamic reciprocity of nuclear ß-catenin, p300/CREB binding protein, and transcriptional initiation factor 2/GC receptor-interaction protein, thereby facilitating hormone-dependent coactivation and transrepression. ß-Catenin responds in an equally dynamic manner with other NRs, including the retinoic acid (RA) receptor (RAR), vitamin D receptor (VDR), glucocorticoid receptor (GR), progesterone receptor, thyroid receptor (TR), estrogen receptor (ER), and peroxisome proliferator-activated receptor (PPAR). The NR ligands, vitamin D3, trans/cis RA, glucocorticoids, and thiazolidines, induce dramatic changes in the physiology of cells harboring high Wnt/ß-catenin/Tcf activity. Wnt signaling regulates, directly or indirectly, developmental processes such as ductal branching and adipogenesis, two processes dependent on NR function. ß-Catenin has been intensively studied in colorectal cancer; however, it is now evident that ß-catenin may be important in cancers of the breast, prostate, and thyroid. This review will focus on the cross-regulation of AR and Wnt/ß-catenin/Tcf but will also consider the dynamic manner in which RAR/RXR, GR, TR, VDR, ER, and PPAR modulate canonical Wnt signaling. Although many commonalities exist by which NRs interact with the Wnt/ß-catenin signaling pathway, striking cell line and tissue-specific differences require deciphering and application to endocrine pathology.




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