Sodium selenite inhibits interleukin-6-mediated androgen receptor activation in prostate cancer cells via upregulation of c-Jun.
Open accessAbstract
Background It has been suggested that interleukin-6 (IL-6) may modulate androgen receptor (AR) action to accelerate prostate cancer (PCa) progression. Selenium compounds are highly recommended as a promising chemopreventive agent for PCa. This study was to determine if selenium can repress IL-6 mediated AR action in PCa progression.Methods Cell proliferation, prostate-specific antigen, gene transfer, and Western blot assays were used to study the effects of sodium selenite and methylseleninic acid on IL-6 mediated AR action on an AR expressing human prostate cancer cell line, LNCaP.Results We found that sodium selenite, but not methylseleninic acid, significantly (p<0.05) inhibited IL-6-induced trans-activating activity of AR and cell proliferation in LNCaP cells. Interestingly, although sodium selenite did not show effect on activation of both STAT3 and ERK1/2 in the presence of IL-6, an increased expression of c-Jun was detected in cells after treatment with sodium selenite. Indeed, we showed overexpression of c-Jun blocked IL-6-induced AR activation.Conclusions Taken together, our results suggest that sodium selenite not methylseleninic acid can inhibit IL-6-mediated AR activation by increased c-Jun in LNCaP cells. Sodium selenite may be a proper selenium form for further testing its potency on intervening IL-6-mediated PCa progression.
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IL-6 stimulation of AR activity in this context can be inhibited by the selenium chemopreventative sodium selenite.
“Interestingly, IL-6 stimulation of AR activity in this context can be inhibited by a form of selenium chemopreventative, sodium selenite (25).”
From Minireview: Alternative Activation Pathways for the Androgen Receptor in Prostate Cancer (2011) · cites this paper as [25]
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- Authors
- Gazi, M. H., Gong, A., Donkena, K. V., & Young, C. Y. F.
- Affiliations
- Mayo Clinic (US)
- Corresponding author
- Young, Charles Y.F.
- ORCID
- Young, Charles Y.F.
- Venue
- Clinica Chimica Acta
- Publisher
- Elsevier BV
- Published
- 2007-05
- Volume
- 380
- Issue
- 1-2
- Pages
- 145-150
- ISSN
- 0009-8981 (ISSN-L)
- PMC
- PMC1955324
- OpenAlex
- W2063075325
- Cited by
- 19
- References
- 47
- Citations by year
- 2022: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2016: 1 · 2015: 3 · 2013: 1 · 2012: 2
- FWCI
- 1.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Clinica Chimica Acta (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (R01CA088900, CA89000)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Health Sciences › Nursing › Nutrition and Dietetics › Selenium in Biological Systems
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Toxicology › Organoselenium and organotellurium chemistry
- Keywords
- sodium selenite, methylseleninic acid, selenium, interleukin-6, androgen receptor, prostate cancer, c-Jun, LNCaP cells, chemoprevention, STAT3, ERK1/2, cell proliferation, prostate-specific antigen
- MeSH terms
- Interleukin-6 Inhibitors, Androgens, Humans, Male, Prostatic Neoplasms, Receptors, Androgen, Transcription, Genetic, Tumor Cells, Cultured, Blotting, Western, Up-Regulation, Proto-Oncogene Proteins c-jun, Prostate-Specific Antigen, Genes, Reporter, Sodium Selenite, Receptors, Interleukin-6, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Cell Proliferation, STAT3 Transcription Factor
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