Phosphorylation and activation of androgen receptor by Aurora-A.
Open accessAbstract
Aurora-A kinase is frequently overexpressed/activated in various types of human malignancy, including prostate cancer. In this study, we demonstrate elevated levels of Aurora-A in androgen-refractory LNCaP-RF but not androgen-sensitive LNCaP cells, which prompted us to examine whether Aurora-A regulates the androgen receptor (AR) and whether elevated Aurora-A is involved in androgen-independent cell growth. We show that ectopic expression of Aurora-A induces AR transactivation activity in the presence and absence of androgen. Aurora-A interacts with AR and phosphorylates AR at Thr(282) and Ser(293) in vitro and in vivo. Aurora-A induces AR transactivation activity in a phosphorylation-dependent manner. Ectopic expression of Aurora-A in LNCaP cells induces prostate-specific antigen expression and cell survival, whereas knockdown of Aurora-A sensitizes LNCaP-RF cells to apoptosis and cell growth arrest. These data indicate that AR is a substrate of Aurora-A and that elevated Aurora-A could contribute to androgen-independent cell growth by phosphorylation and activation of AR.
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Aurora-A expression is elevated in prostate tumors compared with normal tissue.
“Aurora-A expression is elevated in prostate tumors compared with normal tissue.”
From Minireview: Alternative Activation Pathways for the Androgen Receptor in Prostate Cancer (2011) · cites this paper as [57]
Aurora-A can phosphorylate the AR at Thr-282 and Ser-293, leading to transactivation of the receptor.
“Also, Aurora-A, a kinase involved in mitosis progression, can phosphorylate the AR at Thr-282 and Ser-293, leading to transactivation of the receptor (57).”
From Minireview: Alternative Activation Pathways for the Androgen Receptor in Prostate Cancer (2011) · cites this paper as [57]
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Minireview: Alternative Activation Pathways for the Androgen Receptor in Prostate Cancer
Lamont, K. R., & Tindall, D. J. (2011) · Molecular Endocrinology · doi:10.1210/me.2010-0469 · Cited by 150 · see citing works
- Authors
- Shu, S.-K., Liu, Q., Coppola, D., & Cheng, J. Q.
- Affiliations
- Moffitt Cancer Center (US)
- Corresponding author
- Cheng, Jin Q.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2010-10
- Volume
- 285
- Issue
- 43
- Pages
- 33045-33054
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC2963369
- OpenAlex
- W2093863429
- Cited by
- 38
- References
- 51
- Citations by year
- 2022: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 1 · 2017: 5 · 2016: 3 · 2015: 3 · 2014: 3 · 2013: 7 · 2012: 6
- FWCI
- 5.05
- Type
- journal article
- Language
- en
- Status
- Retracted
- Update notices
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (CA137041)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Keywords
- AURKA, androgen receptor, receptor phosphorylation, prostate cancer, androgen-refractory prostate cancer, LNCaP cells, prostate-specific antigen, apoptosis, growth arrest, kinase substrates
- MeSH terms
- Androgens, Gene Expression Regulation, Humans, Male, Phosphorylation, Receptors, Androgen, Transcriptional Activation, Apoptosis, Protein Serine-Threonine Kinases, Prostate-Specific Antigen, Cell Line, Tumor, Gene Knockdown Techniques, Aurora Kinases
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