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Androgen Receptor Activation in Prostatic Tumor Cell Lines by Insulin-like Growth Factor-I, Keratinocyte Growth Factor, and Epidermal Growth Factor¹

Departments of Urology [Z. C., A. Ho., M. V. C., C. R., G. B., H. K.] and Pathology [A. Hi.], University of Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria, and Department of Pathology, Erasmus University Rotterdam, P.O. Box 178, 3000 DR Rotterdam, The Netherlands [J. T.]

Aberrant activation of the androgen receptor (AR) may be one of the mechanisms which contribute to progression of prostatic carcinoma to an androgen-independent stage. We investigated effects of growth factors on stimulation of the AR-mediated gene transcription in human prostatic tumor cell lines. DU-145 cells, which do not contain endogenous AR, were cotransfected with an androgen-inducible chloramphenicol acetyltransferase (CAT) reporter gene and an AR expression vector. The reporter gene (CAT) was driven either by artificial promoters consisting of one or two androgen-responsive elements in front of a TATA box or by the promoter of the prostate-specific antigen (PSA) gene, a naturally occurring androgen-inducible promoter. Insulin-like growth factor-I (IGF-I), at a concentration of 50 ng/ml, stimulated AR-mediated reporter gene transcription to the same extent as the synthetic androgen methyltrienolone. This growth factor was effective irrespective of the nature of the androgen-inducible promoter. Keratinocyte growth factor (KGF) and epidermal growth factor (EGF), at concentrations of 50 ng/ml, activated CAT reporter gene transcription only in experiments in which the artificial promoter with two androgen-responsive elements was used. Insulin-like growth factor-II and basic fibroblast growth factor displayed no effect on AR-mediated gene transcription. None of the growth factors stimulated reporter gene activity in control experiments when added to cells cotransfected with the CAT gene and an empty expression vector. AR activation by IGF-I, KGF, and EGF was completely inhibited by the pure AR antagonist casodex, showing that these effects are AR mediated. Activation of endogenous AR by growth factors was studied in the LNCaP cell line by determination of PSA secretion. IGF-I, at a concentration of 50 ng/ml, increased the PSA level in the supernatant of this cell line 5-fold. Again, the IGF-I effect on PSA secretion was blocked by casodex. Our results provide evidence that IGF-I, KGF, and EGF directly activate the AR in the absence of androgens, which means that the androgen-signaling chain may be activated by growth factors in an androgen-depleted environment. These findings may have implications for endocrine therapy for metastatic prostatic carcinoma.

¹ Supported by Grant SFB F203 of the Austrian Research Funds.

² To whom requests for reprints should be addressed, at Department of Urology, University of Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria.

Received 5/13/94. Accepted 8/17/94.

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				M. Letsch, A. V. Schally, R. Busto, A. M. Bajo, and J. L. Varga Growth hormone-releasing hormone (GHRH) antagonists inhibit the proliferation of androgen-dependent and -independent prostate cancers PNAS, February 4, 2003; 100(3): 1250 - 1255. [Abstract] [Full Text] [PDF]

				Z. Kang, A. Pirskanen, O. A. Janne, and J. J. Palvimo Involvement of Proteasome in the Dynamic Assembly of the Androgen Receptor Transcription Complex J. Biol. Chem., December 6, 2002; 277(50): 48366 - 48371. [Abstract] [Full Text] [PDF]

				R. M. Adam, J. Kim, J. Lin, A. Orsola, L. Zhuang, D. C. Rice, and M. R. Freeman* Heparin-Binding Epidermal Growth Factor-Like Growth Factor Stimulates Androgen-Independent Prostate Tumor Growth and Antagonizes Androgen Receptor Function Endocrinology, December 1, 2002; 143(12): 4599 - 4608. [Abstract] [Full Text] [PDF]

				A. J. James, I. U. Agoulnik, J. M. Harris, G. Buchanan, W. D. Tilley, M. Marcelli, D. J. Lamb, and N. L. Weigel A Novel Androgen Receptor Mutant, A748T, Exhibits Hormone Concentration-Dependent Defects in Nuclear Accumulation and Activity Despite Normal Hormone-Binding Affinity Mol. Endocrinol., December 1, 2002; 16(12): 2692 - 2705. [Abstract] [Full Text] [PDF]

				Y.-F. Lee, W.-J. Lin, J. Huang, E. M. Messing, F. L. Chan, G. Wilding, and C. Chang Activation of Mitogen-activated Protein Kinase Pathway by the Antiandrogen Hydroxyflutamide in Androgen Receptor-negative Prostate Cancer Cells Cancer Res., November 1, 2002; 62(21): 6039 - 6044. [Abstract] [Full Text] [PDF]

				T. Ueda, N. R. Mawji, N. Bruchovsky, and M. D. Sadar Ligand-independent Activation of the Androgen Receptor by Interleukin-6 and the Role of Steroid Receptor Coactivator-1 in Prostate Cancer Cells J. Biol. Chem., October 4, 2002; 277(41): 38087 - 38094. [Abstract] [Full Text] [PDF]

				I. K. Mellinghoff, C. Tran, and C. L. Sawyers Growth Inhibitory Effects of the Dual ErbB1/ErbB2 Tyrosine Kinase Inhibitor PKI-166 on Human Prostate Cancer Xenografts Cancer Res., September 15, 2002; 62(18): 5254 - 5259. [Abstract] [Full Text] [PDF]

				E. D. Martinez and M. Danielsen Loss of Androgen Receptor Transcriptional Activity at the G1/S Transition J. Biol. Chem., August 9, 2002; 277(33): 29719 - 29729. [Abstract] [Full Text] [PDF]

				S. Godoy-Tundidor, A. Hobisch, K. Pfeil, G. Bartsch, and Z. Culig Acquisition of Agonistic Properties of Nonsteroidal Antiandrogens after Treatment with Oncostatin M in Prostate Cancer Cells Clin. Cancer Res., July 1, 2002; 8(7): 2356 - 2361. [Abstract] [Full Text] [PDF]

				J. Dai, R. Shen, M. Sumitomo, R. Stahl, D. Navarro, M. C. Gershengorn, and D. M. Nanus Synergistic Activation of the Androgen Receptor by Bombesin and Low-Dose Androgen Clin. Cancer Res., July 1, 2002; 8(7): 2399 - 2405. [Abstract] [Full Text] [PDF]

				G. G. Giles, G. Severi, R. Sinclair, D. R. English, M. R. E. McCredie, W. Johnson, P. Boyle, and J. L. Hopper Androgenetic Alopecia and Prostate Cancer: Findings from an Australian Case-Control Study Cancer Epidemiol. Biomarkers Prev., June 1, 2002; 11(6): 549 - 553. [Abstract] [Full Text] [PDF]

				Z.-Q. Huang, J. Li, and J. Wong AR Possesses an Intrinsic Hormone-Independent Transcriptional Activity Mol. Endocrinol., May 1, 2002; 16(5): 924 - 937. [Abstract] [Full Text] [PDF]

				D. B. Solit, F. F. Zheng, M. Drobnjak, P. N. Munster, B. Higgins, D. Verbel, G. Heller, W. Tong, C. Cordon-Cardo, D. B. Agus, et al. 17-Allylamino-17-demethoxygeldanamycin Induces the Degradation of Androgen Receptor and HER-2/neu and Inhibits the Growth of Prostate Cancer Xenografts Clin. Cancer Res., May 1, 2002; 8(5): 986 - 993. [Abstract] [Full Text] [PDF]

				T. Karashima, P. Sweeney, J. W. Slaton, S. J. Kim, D. Kedar, J. I. Izawa, Z. Fan, C. Pettaway, D. J. Hicklin, T. Shuin, et al. Inhibition of Angiogenesis by the Antiepidermal Growth Factor Receptor Antibody ImClone C225 in Androgen-independent Prostate Cancer Growing Orthotopically in Nude Mice Clin. Cancer Res., May 1, 2002; 8(5): 1253 - 1264. [Abstract] [Full Text] [PDF]

				T. Ueda, N. Bruchovsky, and M. D. Sadar Activation of the Androgen Receptor N-terminal Domain by Interleukin-6 via MAPK and STAT3 Signal Transduction Pathways J. Biol. Chem., February 22, 2002; 277(9): 7076 - 7085. [Abstract] [Full Text] [PDF]

				F. Barletta, L. P. Freedman, and S. Christakos Enhancement of VDR-Mediated Transcription by Phosphorylation: Correlation with Increased Interaction Between the VDR and DRIP205, a Subunit of the VDR-Interacting Protein Coactivator Complex Mol. Endocrinol., February 1, 2002; 16(2): 301 - 314. [Abstract] [Full Text] [PDF]