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Carcinogenesis |
Departments of Pediatrics [C. W. G., R. T. J., F. S. F., E. M. W.], Surgery (Division of Urology) [J. L. M.], Pathology and Laboratory Medicine [J. L. M.], and Biochemistry/Biophysics [E. M. W.]; The Laboratories for Reproductive Biology [C. W. G., R. T. J., J. L. M., F. S. F., E. M. W.]; and the Lineberger Comprehensive Cancer Center [C. W. G., J. L. M., F. S. F., E. M. W.], The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599
The androgen receptor (AR) is highly expressed in androgen-dependent and recurrent prostate cancer (CaP) suggesting it has a role in the growth and progression of CaP. Previously proposed mechanisms for AR reactivation in recurrent CaP include altered growth factor signaling leading to protein phosphorylation and AR mutations that broaden ligand specificity. To further establish a role for AR in recurrent CaP, we compared several properties of AR in relation to the growth response to low levels of androgens in model systems of androgen-dependent and recurrent CaP. AR from all of the tumors and cell lines bound [3H]R1881 with similar high affinity (mean Kd, 0.12 nM). In the absence of androgen, AR in androgen-dependent LNCaP cells was unstable with a degradation half-time (t1/2) of 3 h at 37°C. In contrast, AR was 2–4 times more stable in recurrent CWR22 tumors (t1/2, >12 h) and CWR-R1 or LNCaP-C4-2 cell lines (t1/2, 6–7 h) derived from recurrent prostate tumors. In the recurrent CWR22 tumor and its CWR-R1 cell line grown in the absence of androgen, AR immunostaining was entirely nuclear, whereas under the same conditions AR in LNCaP-C4-2 and LNCaP cells was predominantly nuclear but was also detected in the cytoplasm. High level expression, increased stability, and nuclear localization of AR in recurrent tumor cells were associated with an increased sensitivity to the growth-promoting effects of dihydrotestosterone in the femtomolar range. The concentration of dihydrotestosterone required for growth stimulation in CWR-R1 and LNCaP-C4-2 cells was four orders of magnitude lower than that required for androgen-dependent LNCaP cells. The results suggest that AR is transcriptionally active in recurrent CaP and can increase cell proliferation at the low circulating levels of androgen reported in castrated men.
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 K-M Rau, H-Y Kang, T-L Cha, S A Miller, and M-C Hung The mechanisms and managements of hormone-therapy resistance in breast and prostate cancers Endocr. Relat. Cancer, September 1, 2005; 12(3): 511 - 532. [Abstract] [Full Text] [PDF]
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 S. Bai, B. He, and E. M. Wilson Melanoma Antigen Gene Protein MAGE-11 Regulates Androgen Receptor Function by Modulating the Interdomain Interaction Mol. Cell. Biol., February 15, 2005; 25(4): 1238 - 1257. [Abstract] [Full Text] [PDF]
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J. Holzbeierlein, P. Lal, E. LaTulippe, A. Smith, J. Satagopan, L. Zhang, C. Ryan, S. Smith, H. Scher, P. Scardino, et al. Gene Expression Analysis of Human Prostate Carcinoma during Hormonal Therapy Identifies Androgen-Responsive Genes and Mechanisms of Therapy Resistance Am. J. Pathol., January 1, 2004; 164(1): 217 - 227. [Abstract] [Full Text] [PDF]
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B. Comuzzi, L. Lambrinidis, H. Rogatsch, S. Godoy-Tundidor, N. Knezevic, I. Krhen, Z. Marekovic, G. Bartsch, H. Klocker, A. Hobisch, et al. The Transcriptional Co-Activator cAMP Response Element-Binding Protein-Binding Protein Is Expressed in Prostate Cancer and Enhances Androgen- and Anti-Androgen-Induced Androgen Receptor Function Am. J. Pathol., January 1, 2003; 162(1): 233 - 241. [Abstract] [Full Text] [PDF]
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C. G. Tepper, D. L. Boucher, P. E. Ryan, A.-H. Ma, L. Xia, L.-F. Lee, T. G. Pretlow, and H.-J. Kung Characterization of a Novel Androgen Receptor Mutation in a Relapsed CWR22 Prostate Cancer Xenograft and Cell Line Cancer Res., November 15, 2002; 62(22): 6606 - 6614. [Abstract] [Full Text] [PDF]
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 Y. Lukyanenko, J.-J. Chen, and J. C. Hutson Testosterone Regulates 25-Hydroxycholesterol Production in Testicular Macrophages Biol Reprod, November 1, 2002; 67(5): 1435 - 1438. [Abstract] [Full Text] [PDF]
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D. Wu and D. M. Terrian Regulation of Caveolin-1 Expression and Secretion by a Protein Kinase Cepsilon Signaling Pathway in Human Prostate Cancer Cells J. Biol. Chem., October 18, 2002; 277(43): 40449 - 40455. [Abstract] [Full Text] [PDF]
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D. Gioeli, S. B. Ficarro, J. J. Kwiek, D. Aaronson, M. Hancock, A. D. Catling, F. M. White, R. E. Christian, R. E. Settlage, J. Shabanowitz, et al. Androgen Receptor Phosphorylation. REGULATION AND IDENTIFICATION OF THE PHOSPHORYLATION SITES J. Biol. Chem., August 2, 2002; 277(32): 29304 - 29314. [Abstract] [Full Text] [PDF]
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M. A. Eid, R. W. Lewis, and M. V. Kumar Mifepristone Pretreatment Overcomes Resistance of Prostate Cancer Cells to Tumor Necrosis Factor {alpha}-related Apoptosis-inducing Ligand (TRAIL) Mol. Cancer Ther., August 1, 2002; 1(10): 831 - 840. [Abstract] [Full Text] [PDF]
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E. P. Gelmann Molecular Biology of the Androgen Receptor J. Clin. Oncol., July 1, 2002; 20(13): 3001 - 3015. [Abstract] [Full Text] [PDF]
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C. D. Chen and C. L. Sawyers NF-{kappa}B Activates Prostate-Specific Antigen Expression and Is Upregulated in Androgen-Independent Prostate Cancer Mol. Cell. Biol., April 15, 2002; 22(8): 2862 - 2870. [Abstract] [Full Text] [PDF]
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D. Kim, C. W. Gregory, F. S. French, G. J. Smith, and J. L. Mohler Androgen Receptor Expression and Cellular Proliferation During Transition from Androgen-Dependent to Recurrent Growth after Castration in the CWR22 Prostate Cancer Xenograft Am. J. Pathol., January 1, 2002; 160(1): 219 - 226. [Abstract] [Full Text] [PDF]
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H. Murillo, H. Huang, L. J. Schmidt, D. I. Smith, and D. J. Tindall Role of PI3K Signaling in Survival and Progression of LNCaP Prostate Cancer Cells to the Androgen Refractory State Endocrinology, November 1, 2001; 142(11): 4795 - 4805. [Abstract] [Full Text] [PDF]
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C. W. Gregory, B. He, R. T. Johnson, O. H. Ford, J. L. Mohler, F. S. French, and E. M. Wilson A Mechanism for Androgen Receptor-mediated Prostate Cancer Recurrence after Androgen Deprivation Therapy Cancer Res., June 1, 2001; 61(11): 4315 - 4319. [Abstract] [Full Text] [PDF]
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