The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Androgen receptors in prostate cancer.
Open accessAbstract
The androgen receptor (AR), a transcription factor that mediates the action of androgens in target tissues, is expressed in nearly all prostate cancers. Carcinoma of the prostate is the most frequently diagnosed neoplasm in men in industrialized countries. Palliative treatment for non-organ-confined prostate cancer aims to down-regulate the concentration of circulating androgen or to block the transcription activation function of the AR. AR function during endocrine therapy was studied in tumor cells LNCaP subjected to long-term steroid depletion; newly generated sublines could be stimulated by lower concentrations of androgen than parental cells and showed up-regulation of AR expression and activity as well as resistance to apoptosis. Androgenic hormones regulate the expression of key cell cycle regulators, cyclin-dependent kinase 2 and 4, and that of the cell cycle inhibitor p27. Inhibition of AR expression could be achieved by potential chemopreventive agents flufenamic acid, resveratrol, quercetin, polyunsaturated fatty acids and interleukin-1beta, and by the application of AR antisense oligonucleotides. In the clinical situation, AR gene amplification and point mutations were reported in patients with metastatic disease. These mutations generate receptors which could be activated by other steroid hormones and non-steroidal antiandrogens. In the absence of androgen, the AR could be activated by various growth-promoting (growth factors, epidermal growth factor receptor-related oncogene HER-2/neu) and pleiotropic (protein kinase A activators, interleukin-6) compounds as well as by inducers of differentiation (phenylbutyrate). AR function is modulated by a number of coactivators and corepressors. The three coactivators, TIF-2, SRC-1 and RAC3, are up-regulated in relapsed prostate cancer. New experimental therapies for prostate cancer are aimed to down-regulate AR expression and to overcome difficulties which occur because of the acquisition of agonistic properties of commonly used antiandrogens.
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Cites
In vivo amplification of the androgen receptor gene and progression of human prostate cancer
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The Roles of Androgen Receptors and Androgen-Binding Proteins in Nongenomic Androgen Actions
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“Gross deletions in the ligand-binding domain of the AR generate receptors which are constitutively active (Jenster et al. 1991).”
BackgroundLinking β-Catenin to Androgen-signaling Pathway
Yang, F., Li, X., Sharma, M., Sasaki, C. Y., Longo, D. L., Lim, B., & Sun, Z. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m111962200 · Cited by 342
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Cited by
Guo, Z., Yang, X., Sun, F., Jiang, R., Linn, D. E., Chen, H., Chen, H., Kong, X., Melamed, J., Tepper, C. G., et al. (2009) · Cancer Research · doi:10.1158/0008-5472.can-08-3795 · Cited by 880
TCF/LEFs and Wnt Signaling in the Nucleus
Cadigan, K. M., & Waterman, M. L. (2012) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a007906 · Cited by 760
Interleukin-6 regulation of prostate cancer cell growth.
Culig, Z., Steiner, H., Bartsch, G., & Hobisch, A. (2005) · Journal of Cellular Biochemistry · doi:10.1002/jcb.20477 · Cited by 269
Self-citationMemarzadeh, S., Xin, L., Mulholland, D. J., Mansukhani, A., Wu, H., Teitell, M. A., & Witte, O. N. (2007) · Cancer Cell · doi:10.1016/j.ccr.2007.11.002 · Cited by 201
Moon, J.-S., Jin, W.-J., Kwak, J.-H., Kim, H.-J., Yun, M.-J., KIM, J.-W., Park, S. W., & Kim, K.-S. (2011) · Biochemical Journal · doi:10.1042/bj20101104 · Cited by 125
Metadata
- Authors
- Culig, Z., Klocker, H., Bartsch, G., & Hobisch, A.
- Venue
- Endocrine-related cancer
- Publisher
- Bioscientifica
- Published
- 2002-09
- Volume
- 9
- Issue
- 3
- Pages
- 155-170
- ISSN
- 1351-0088 (ISSN-L)
- OpenAlex
- W2033281378
- Cited by
- 247
- References
- 7
- FWCI
- 12.78
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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