Androgen Mediated Regulation of the G1-S Transition in Prostate Cancer
Prostatic adenocarcinoma is the most frequently diagnosed malignancy in the United States and is the second leading cause of cancer deaths among men (Landis et al., 1998). Most prostate cancers are treated by androgen ablation, since androgen is a required mitogen for the survival and proliferation of prostate cells (Cunha et al., 1987; Jenster, 1999; Klotz, 2000; Labrie, 2000). This treatment is initially effective, as upon androgen withdrawal most prostate cancer cells undergo cell cycle arrest or cell death (Denmeade et al., 1996; Murphy et al., 1991; Westin et al., 1995). Unfortunately, androgen independent tumors arise and lead to patient morbidity. Determination of how androgen exerts its effect as a mitogen in early prostate cancer, and how the androgen requirement is subverted in advanced disease is the focus of intensive research.
KeywordsProstate Cancer Androgen Receptor Prostate Cancer Cell LNCaP Cell Kinase Assay
Unable to display preview. Download preview PDF.
- Baretton, G.B., Klenk, U., Diebold, J., Schmeller, N., and Lohrs, U. 1999. Proliferation-and apoptosis-associated factors in advanced prostatic carcinomas before and after androgen deprivation therapy: prognostic significance of p21/WAFl/CIPl expression. Br J Cancer 80, 546–55.PubMedCrossRefGoogle Scholar
- Cordon-Cardo, C., Koff, A., Drobnjak, M., Capodieci, P., Osman, I., Millard, S.S., Gaudin, P. B., Fazzari, M., Zhang, Z.F., Massague, J., and Scher, H.I. 1998. Distinct altered patterns of p27KIPl gene expression in benign prostatic hyperplasia and prostatic carcinoma. J Natl Cancer Inst 90, 1284–91.PubMedCrossRefGoogle Scholar
- Culig, Z., Hobisch, A., Cronauer, M.V., Radmayr, C., Trapman, J., Hittmair, A., Bartsch, G., and Klocker, H. 1994. Androgen receptor activation in prostatic tumor cell lines by insulin-like growth factor-I, keratinocyte growth factor, and epidermal growth factor. Cancer Res 54, 5474–8.PubMedGoogle Scholar
- Di Cristofano. A., Pesce, B., Cordon-Cardo, C, Pandolfi, P.P. Pten is essential for embryonic development and tumor suppression. Nat Genet 19, 348–55Google Scholar
- Henshall, S.M., Quinn, D.I., Lee, C.S., Head, D.R., Golovsky, D., Brenner, P.C., Delprado, W., Strieker, P.D., Grygiel, J.J., and Sutherland, R.L. 2001. Overexpression of the cell cycle inhibitor pl6INK4A in high-grade prostatic intraepithelial neoplasia predicts early relapse in prostate cancer patients. Clin Cancer Res 7, 544–50.PubMedGoogle Scholar
- Jarrard, D.F., Sarkar, S., Shi, Y., Yeager, T.R., Magrane, G., Kinoshita, H., Nassif, N., Meisner, L., Newton, M.A., Waldman, F.M., and Reznikoff, C.A. 1999. pl6/pRb pathway alterations are required for bypassing senescence in human prostate epithelial cells. Cancer Res 59, 2957–64.PubMedGoogle Scholar
- Li, P, Nicosia, S.V., and Bai, W. 2001. Antagonism between PTEN/MMAC1/TEP-1 and androgen receptor in growth and apoptosis of prostatic cancer cells. J. Biol. Chem. 16 March.Google Scholar
- Lukas, J., Muller, H., Bartkova, J., Spitkovsky, D., Kjerulff, A.A., Jansen-Durr, P., Strauss, M., and Bartek, J. 1994. DNA tumor virus oncoproteins and retinoblastoma gene mutations share the ability to relieve the cell’s requirement for cyclin Dl function in Gl. J Cell Biol 125, 625–38.PubMedCrossRefGoogle Scholar
- Mashai, R.D., Lester, S., Corless, C, Richie, J.P., Chandra, R., Propert, K.J., and Dutta, A. 1996. Expression of cell cycle-regulated proteins in prostate cancer. Cancer Res 56, 4159–63.Google Scholar
- Masumori, N., Thomas, T.Z., Chaurand, P., Case, T., Paul, M., Kasper, S., Caprioli, R.M., Tsukamoto, T., Shappell, S.B., and Matusik, R.J. 2001. A probasin-large T antigen transgenic mouse line develops prostate adenocarcinoma and neuroendocrine carcinoma with metastatic potential. Cancer Res 61, 2239–49.PubMedGoogle Scholar
- Yeh, S., Lin, H.K., Kang, H Y., Thin, T.H., Lin, M.F., and Chang, C. 1999. From HER2/Neu signal cascade to androgen receptor and its coactivators: a novel pathway by induction of androgen target genes through MAP kinase in prostate cancer cells. Proc Natl Acad Sei USA 96, 5458–63.CrossRefGoogle Scholar