Regulation of androgen receptor activity by tyrosine phosphorylation.
Open accessAbstract
The androgen receptor (AR) is essential for the growth of prostate cancer cells. Here, we report that tyrosine phosphorylation of AR is induced by growth factors and elevated in hormone-refractory prostate tumors. Mutation of the major tyrosine phosphorylation site in AR significantly inhibits the growth of prostate cancer cells under androgen-depleted conditions. The Src tyrosine kinase appears to be responsible for phosphorylating AR, and there is a positive correlation of AR tyrosine phosphorylation with Src tyrosine kinase activity in human prostate tumors. Our data collectively suggest that growth factors and their downstream tyrosine kinases, which are elevated during hormone-ablation therapy, can induce tyrosine phosphorylation of AR and such modification may be important for prostate tumor growth under androgen-depleted conditions.
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Activated Src can phosphorylate the AR at Tyr-534, thereby promoting its transcriptional activity in LNCaP and LAPC-4 cells.
“Activated Src can phosphorylate AR at Tyr-534, thereby promoting its transcriptional activity in LNCaP and LAPC-4 cells (27,28).”
From Minireview: Alternative Activation Pathways for the Androgen Receptor in Prostate Cancer (2011) · cites this paper as [27]
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- Authors
- Guo, Z., Dai, B., Jiang, T., Xu, K., Xie, Y., Kim, O., Nesheiwat, I., Kong, X., Melamed, J., Handratta, V. D., Njar, V. C. O., Brodie, A. M. H., Yu, L.-R., Veenstra, T. D., Chen, H., & Qiu, Y.
- Affiliations
- University of Maryland, Baltimore (US)
- New York University (US)
- National Cancer Institute (US)
- Corresponding author
- Qiu, Yun
- ORCID
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2006-10
- Volume
- 10
- Issue
- 4
- Pages
- 309-319
- ISSN
- 1535-6108 (ISSN-L)
- OpenAlex
- W2078400569
- Cited by
- 364
- References
- 54
- Citations by year
- 2025: 4 · 2024: 5 · 2023: 11 · 2022: 12 · 2021: 14 · 2020: 7 · 2019: 10 · 2018: 13 · 2017: 20 · 2016: 21 · 2015: 32 · 2014: 22 · 2013: 31 · 2012: 28
- FWCI
- 19.43
- Type
- journal article
- Language
- en
- Update notices
- erratum (2007-01-01)
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- DigitalCommons-Cedarville (Cedarville University) (submittedVersion)
- Funders
- Prostate Cancer Foundation
- National Institutes of Health (n01co12400-79-0-22, 5r01ca085380-06)
- National Cancer Institute (N01CO12400, U01 CA86772, CA 85380, CA106504, R01CA106504, U01CA086772)
- National Institute of Environmental Health Sciences (T32ES007263, T32 ES07263)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Keywords
- androgen receptor, tyrosine phosphorylation, Src kinase, prostate cancer, castration-resistant prostate cancer, growth factors, hormone ablation therapy, tyrosine kinase inhibitors
- MeSH terms
- Androgens, Animals, Chlorocebus aethiops, Epidermal Growth Factor, Humans, Immunohistochemistry, Indoles, Kinetics, Male, Phosphorylation, Prostatic Neoplasms, Pyrimidines, Receptors, Androgen, Dihydrotestosterone, Sulfonamides, Tyrosine, Interleukin-6, Gene Expression Regulation, Neoplastic, Mice, SCID, src-Family Kinases, COS Cells, Neuregulin-1, Xenograft Model Antitumor Assays, Cell Line, Tumor, Mice
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