Cited by 151Wnt/β-catenin signaling in development and cancerProstate Cancer Treatment and ResearchSignaling Pathways in Disease

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Ligand-dependent inhibition of β-catenin/TCF signaling by androgen receptor

Chesire, Dennis R, Isaacs, William B·2002·Oncogene

DOI 10.1038/sj.onc.1206049

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Abstract

Beta-catenin signaling may contribute to prostate cancer (CaP) progression. Although beta-catenin is known to upregulate T cell factor (TCF) target gene expression in CaP cells, recent evidence demonstrates its capacity to enhance ligand-dependent androgen receptor (AR) function. Thus, we wished to further understand the interaction between these two pathways. We find in both CaP cells (CWR22-Rv1, LAPC-4, DU145) and non-CaP cells (HEK-293, TSU, SW480, HCT-116) that beta-catenin/TCF-related transcription (CRT), as measured by activation of a synthetic promoter and that of cyclin D1, is inhibited by androgen treatment. This inhibition is AR-dependent, as it only occurs in cells expressing AR endogenously or transiently, and is abrogated by AR antagonists. Additional analyses convey that the ligand-dependent nature of CRT suppression depends on transactivation-competent AR in the nucleus, but not on indirect effects stemming from AR target gene expression. Given the recent work identifying an AR/beta-catenin interaction, and from our finding that liganded AR does not prompt gross changes in the constitutive nuclear localization of TCF4 or mutant beta-catenin, we hypothesized that transcription factor (i.e. AR and TCF) competition for beta-catenin recruitment may explain, in part, androgen-induced suppression of CRT. To address this idea, we expressed an AR mutant lacking its DNA-binding domain (DBD). This receptor could not orchestrate ligand-dependent CRT repression, thereby providing support for those recent data implicating the AR DBD/LBD as necessary for beta-catenin interaction. Further supporting this hypothesis, TCF/LEF over-expression counteracts androgen-induced suppression of CRT, and requires beta-catenin binding activity to do so. Interestingly, TCF4 over-expression potently antagonizes AR function; however, this inhibition may occur independently of beta-catenin/TCF4 interaction. These results from TCF4 over-expression analyses, taken together, provide further evidence that AR-mediated suppression of CRT is a consequence of limiting amounts of beta-catenin, and not AR target gene expression. Our analyses point to a reciprocal balance between AR and CRT function that may shape critical processes during normal prostate development and tumor progression.

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See all 151

Authors: Chesire, D. R., & Isaacs, W. B.
Affiliations: Johns Hopkins University (US)
Corresponding author: Isaacs, William B
ORCID: Isaacs, William B
Venue: Oncogene
Publisher: Springer Science and Business Media LLC
Published: 2002-12-04
Volume: 21
Issue: 55
Pages: 8453-8469
ISSN: 0950-9232 (ISSN-L)
1476-5594
DOI: 10.1038/sj.onc.1206049
OpenAlex: W1970833195
Cited by: 151
References: 93
Citations by year: 2026: 3 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 3 · 2021: 8 · 2020: 4 · 2019: 7 · 2018: 2 · 2017: 9 · 2016: 5 · 2015: 5 · 2014: 8 · 2013: 9 · 2012: 10
FWCI: 3.36
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Oncogene (publishedVersion)
PubMed (publishedVersion)
Funders: National Cancer Institute (CA58236, P50CA058236)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Prostate Cancer Treatment and Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
Keywords: androgen receptor, β-catenin, TCF/LEF, Wnt signaling, prostate cancer, ligand-dependent transcription, transcription factor competition, TCF4, cyclin D1, DNA-binding domain, transcriptional repression
MeSH terms: Animals, Cell Line, Cell Nucleus, Cytoskeletal Proteins, DNA-Binding Proteins, Humans, Ligands, Male, Prostatic Neoplasms, Receptors, Androgen, Transcription Factors, Transcription, Genetic, Tumor Cells, Cultured, Signal Transduction, Trans-Activators, beta Catenin, TCF Transcription Factors, Transcription Factor 7-Like 2 Protein

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Ligand-dependent inhibition of β-catenin/TCF signaling by androgen receptor

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