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Molecular cell biology of androgen receptor signalling
Abstract
The classical action of androgen receptor (AR) is to regulate gene transcriptional processes via AR nuclear translocation, response element binding and recruitment of, or crosstalk with, transcription factors. AR also utilises non-classical, non-genomic mechanisms of signal transduction. These precede gene transcription or protein synthesis, and involve steroid-induced modulation of cytoplasmic or cell membrane-bound regulatory proteins. Despite many decades of investigation, the role of AR in gene regulation of cells and tissues remains only partially characterised. AR exerts most of its effects in sex hormone-dependent tissues of the body, but the receptor is also expressed in many tissues not previously thought to be androgen sensitive. Thus it is likely that a complex, more over-arching, role for AR exists. Each AR domain co-ordinates a multitude of individual and vital roles via a diverse array of interacting partner molecules that are necessary for cellular and tissue development and maintenance. Aberrant AR activity, promoted by mutations or binding partner misregulation, can present as many clinical manifestations including androgen insensitivity syndrome and prostate cancer. In the case of malignant prostate cancer, treatment generally revolves around androgen deprivation therapies designed to interfere with AR action and the androgen signalling axis. Androgen therapies for prostate cancer often fail, highlighting a real need for increased research into AR function.
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“Androgen transmits signals via cell membrane receptors [19], which are distinct from the androgen nuclear receptors [20].”
From G protein-coupled receptors function as cell membrane receptors for the steroid hormone 20-hydroxyecdysone (2020) · cites this paper as [20]
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“The AR-ligand complex translocates into the nucleus, where it binds AREs [19].”
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“recognized member of the nuclear receptor (NR) superfamily of ligand-inducible transcription factor (2).”
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“Studies of the X-linked androgen insensitivity syndrome have demonstrated that the same receptor mutation can be associated with complete feminization (“testicular feminization”), partial insensitivity, or minimal perturbations in virilization or fertility (73).”
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“, 2013), and it has been shown that HDAC-1 interacts with the AR (Bennett et al., 2010; Gaughan et al., 2002).”
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TRIM33 drives prostate tumor growth by stabilizing androgen receptor from Skp2‐mediated degradation
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“After activation by androgen, AR translocates to the nucleus, binds to specific AR binding sites (ARBSs), and recruits multiple coregulators in a highly regulated manner (Bennett et al , 2010).”
Androgen Regulates Mafb Expression Through its 3′UTR During Mouse Urethral Masculinization
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Metadata
- Authors
- Bennett, N. C., Gardiner, R. A., Hooper, J. D., Johnson, D. W., & Gobe, G. C.
- Affiliations
- The University of Queensland (AU)
- Queensland University of Technology (AU)
- Princess Alexandra Hospital (AU)
- Corresponding author
- Gobe, Glenda C.
- Venue
- The International Journal of Biochemistry & Cell Biology
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 42
- Issue
- 6
- Pages
- 813-827
- ISSN
- 1357-2725 (ISSN-L)
- OpenAlex
- W1546185806
- Cited by
- 292
- References
- 172
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 16 · 2023: 18 · 2022: 24 · 2021: 22 · 2020: 23 · 2019: 17 · 2018: 22 · 2017: 15 · 2016: 13 · 2015: 30 · 2014: 15 · 2013: 22 · 2012: 18
- FWCI
- 2.23
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- The International Journal of Biochemistry & Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Faculty of Health; Institute of Health and Biomedical Innovation
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Prostate Cancer Treatment and Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Keywords
- androgen receptor, androgen signaling, nuclear translocation, transcriptional regulation, transcription factor crosstalk, androgen insensitivity syndrome, prostate cancer, androgen deprivation therapy, androgen receptor mutations
- MeSH terms
- Animals, Humans, Male, Polymorphism, Genetic, Prostatic Neoplasms, Receptors, Androgen, Gonadal Steroid Hormones, Androgen-Insensitivity Syndrome, Transcription Factors, Signal Transduction, Transcriptional Activation, Genetic Predisposition to Disease, Multiprotein Complexes
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