Activation of the androgen receptor N-terminal domain by interleukin-6 via MAPK and STAT3 signal transduction pathways.
Open accessAbstract
The androgen receptor (AR) is a ligand-activated transcription factor that mediates the biological responses of androgens. However, non-androgenic pathways have also been shown to activate the AR. The mechanism of cross-talk between the interleukin-6 (IL-6) and AR signal transduction pathways was investigated in LNCaP human prostate cancer cells. IL-6 induced several androgen-response element-driven reporters that are dependent upon the AR, increased the phosphorylation of mitogen-activated protein kinase (MAPK), and activated the AR N-terminal domain (NTD). Inhibitors to MAPK and JAK decreased the IL-6-induced phosphorylation of MAPK and activation of the AR NTD. Immunoprecipitation and transactivation studies showed a direct interaction between amino acids 234-558 of the AR NTD and STAT3 following IL-6 treatment of LNCaP cells. These results demonstrate that activation of the human AR NTD by IL-6 was mediated through MAPK and STAT3 signal transduction pathways in LNCaP prostate cancer cells.
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STAT3 interacts directly with amino acids 234-558 of the AR, and this interaction is dependent upon phosphorylation of STAT3 at Ser-722.
“STAT3 interacts directly with amino acids 234 -558 of the AR (23), an interaction that is dependent upon phosphorylation of STAT3 at Ser-722 (24).”
From Minireview: Alternative Activation Pathways for the Androgen Receptor in Prostate Cancer (2011) · cites this paper as [23]
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References 82 · Cited by 381
Research works printed but not linked: 4
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- Authors
- Ueda, T., Bruchovsky, N., & Sadar, M. D.
- Affiliations
- BC Cancer Agency (CA)
- Corresponding author
- Sadar, Marianne D.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2002-03
- Volume
- 277
- Issue
- 9
- Pages
- 7076-7085
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W1969241521
- Cited by
- 381
- References
- 82
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 13 · 2023: 13 · 2022: 13 · 2021: 16 · 2020: 8 · 2019: 10 · 2018: 9 · 2017: 12 · 2016: 15 · 2015: 21 · 2014: 15 · 2013: 24 · 2012: 15
- FWCI
- 22.96
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Defense
- National Institutes of Health (5p50dk047656-07)
- U.S. Army
- National Institute of Diabetes and Digestive and Kidney Diseases (P50 DK47656)
- Medical Research and Materiel Command
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Keywords
- androgen receptor, interleukin-6, MAPK signaling, STAT3, signal transduction, prostate cancer, LNCaP cells, JAK inhibitors, transcriptional activation
- MeSH terms
- Amino Acids, Anilides, DNA-Binding Proteins, Dose-Response Relationship, Drug, Enzyme Activation, Colforsin, Humans, Luciferases, Male, Models, Biological, Nitriles, Phosphorylation, Plasmids, Precipitin Tests, Promoter Regions, Genetic, Prostatic Neoplasms, Protein Binding, Protein-Tyrosine Kinases, Receptors, Androgen, Tetrazolium Salts, Thiazoles, Tosyl Compounds, Transfection, Tumor Cells, Cultured, Immunoblotting, Blotting, Northern, Signal Transduction, Transcriptional Activation, Trans-Activators, Interleukin-6, Protein Structure, Tertiary, Reverse Transcriptase Polymerase Chain Reaction, MAP Kinase Signaling System, STAT3 Transcription Factor, Janus Kinase 1
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