Androgen receptor (AR) expression in AR‐negative prostate cancer cells results in differential effects of DHT and IGF‐I on proliferation and AR activity between localized and metastatic tumors
Abstract
Background Two features of the progression from organ-confined to metastatic prostate cancer are dysregulation of the androgen receptor (AR) and a decrease in insulin-like growth factor-type-I receptor (IGF-IR) expression. The purpose of this study was to determine the effect of changes in IGF-IR expression on AR activity. Methods M12 human prostate cells were stably transfected with an AR expression construct to produce the M12-AR parental (PAR) cell line. PAR cells were implanted orthotopically into nude mice and M12-AR primary (PRI) cell lines were derived from intraprostatic tumors and metastatic cell lines (MET) were derived from PRI tumors that had metastasized to diaphragm or lung. Results Tumor formation in the prostate by PAR cells was decreased significantly compared to M12 controls. PAR, PRI, and MET cells expressed equivalent amounts of AR protein; however, IGF-IR expression was increased significantly in PAR and PRI cells. IGF-IR expression decreased in MET lines to the levels seen in M12 control cells. IGF-I significantly enhanced dihydrotestosterone (DHT)-stimulated, but not basal, AR transcriptional activity in PRI cells. In MET cells, IGF-I significantly suppressed DHT-stimulated transcriptional activity. In MET cells in which the IGF-IR was re-expressed from a retroviral vector, the effects of DHT and IGF-I on AR activity were similar to those seen in PRI cells. Conclusions This study demonstrates that the changes in IGF-IR expression exhibited by this model…
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FKBP51 enhances androgen-stimulated transcription from AREs of the probasin promoter.
“FKBP51 enhanced androgen-stimulated transcription measured on AREs from the probasin (22) promoter (AAR3tk-Luc; Fig. 2B)”
From FKBP51 Promotes Assembly of the Hsp90 Chaperone Complex and Regulates Androgen Receptor Signaling in Prostate Cancer Cells (2010) · cites this paper as [22]
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- Authors
- Plymate, S. R., Tennant, M. K., Culp, S. H., Woodke, L., Marcelli, M., Colman, I., Nelson, P. S., Carroll, J. M., Roberts, C. T., & Ware, J. L.
- Affiliations
- University of Washington (US)
- Virginia Commonwealth University (US)
- Baylor College of Medicine (US)
- Fred Hutch Cancer Center (US)
- Oregon Health & Science University (US)
- Corresponding author
- Plymate, Stephen R.
- Venue
- The Prostate
- Publisher
- Wiley
- Published
- 2004-04-22
- Volume
- 61
- Issue
- 3
- Pages
- 276-290
- ISSN
- 0270-4137 (ISSN-L)
- 1097-0045
- OpenAlex
- W1995078013
- Cited by
- 41
- References
- 41
- Citations by year
- 2024: 1 · 2017: 1 · 2016: 1 · 2015: 3 · 2014: 2 · 2013: 3 · 2012: 2
- FWCI
- 3.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Prostate (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (P01CA085859, P01CA85859)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK 52683, R01DK052683)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Health Sciences › Medicine › Reproductive Medicine › Sperm and Testicular Function
- Keywords
- androgen receptor, IGF-1 receptor, insulin-like growth factor I, dihydrotestosterone, prostate cancer metastasis, androgen receptor transcriptional activity, tumor cell proliferation, androgen receptor signaling
- MeSH terms
- Phosphoinositide-3 Kinase Inhibitors, Androgens, Animals, Cell Division, Cell Line, Transformed, Cell Survival, Enzyme Inhibitors, Humans, Insulin-Like Growth Factor I, Male, Mice, Nude, Prostatic Neoplasms, Proto-Oncogene Proteins, Receptors, Androgen, RNA, Messenger, Dihydrotestosterone, Transcription, Genetic, Signal Transduction, Protein Serine-Threonine Kinases, Receptor, IGF Type 1, Phosphatidylinositol 3-Kinases, Mitogen-Activated Protein Kinases, Proto-Oncogene Proteins c-akt, Mice
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