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Titolo:
PROSTATE-CANCER CELL-GROWTH INHIBITION BY TAMOXIFEN IS ASSOCIATED WITH INHIBITION OF PROTEIN-KINASE-C AND INDUCTION OF P21(WAF1 CIP1)/
Autore:
ROHLFF C; BLAGOSKLONNY MV; KYLE E; KESARI A; KIM IY; ZELNER DJ; HAKIM F; TREPEL J; BERGAN RC;
Indirizzi:
NCI,MED BRANCH,NIH,BLDG 10,RM 12N226,9000 ROCKVILLE PIKE BETHESDA MD 20892 NCI,MED BRANCH,NIH BETHESDA MD 20892 NORTHWESTERN UNIV,DEPT UROL CHICAGO IL 60611
Titolo Testata:
The Prostate
fascicolo: 1, volume: 37, anno: 1998,
pagine: 51 - 59
SICI:
0270-4137(1998)37:1<51:PCIBTI>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
FOCAL ADHESION KINASE; BETA TGF-BETA; TRANSFORMING GROWTH-FACTOR-BETA-1; SIGNAL-TRANSDUCTION; ESTROGEN-RECEPTOR; IN-VITRO; EXPRESSION; APOPTOSIS; TUMOR; LINES;
Keywords:
TRANSFORMING GROWTH FACTOR BETA; RETINOBLASTOMA; SIGNAL TRANSDUCTION; DRUG THERAPY; CELL CYCLE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
C. Rohlff et al., "PROSTATE-CANCER CELL-GROWTH INHIBITION BY TAMOXIFEN IS ASSOCIATED WITH INHIBITION OF PROTEIN-KINASE-C AND INDUCTION OF P21(WAF1 CIP1)/", The Prostate, 37(1), 1998, pp. 51-59

Abstract

BACKGROUND. Inhibition of protein kinase C (PKC) and modulation of transforming growth factor-beta (TGF-beta) are both associated with tamoxifen treatment, and both appear to be important in the regulation of prostate cancer cell growth. Investigations were performed which sought to measure the efficacy, and to elucidate the mechanism of growth inhibition by tamoxifen, in hormone-refractory prostate cancer. METHODS. Growth assays were performed on PC3, PC3-M, and DU145 prostate cancercells. TGF-beta was measured by ELISA; p21(waf1/cip1) and retinoblastoma (Rb) protein levels were measured by Western blot; PKC activity was measured by kinase assay; and effects upon cell cycle were measured by flow cytometric analysis. RESULTS. IC(50)s for growth inhibition ranged from 5.5-10 mu M, and were not affected by estrogen. Tamoxifen-mediated growth inhibition was not associated with induction of TGF-beta. However, tamoxifen treatment was associated with inhibition of PKC, which was followed by induction of p2l(waf1/cip1), Rb dephosphorylation, and G1/S phase cell cycle arrest. Similar effects were observed with the known PKC inhibitor, Ro31-8220. CONCLUSIONS. These data suggest that micromolar concentrations of tamoxifen inhibit prostate cancer cell growth by inhibition of PKC, resulting in induction of the p21(waf1/cip1) protein. Prostate 37:51-59, 1998. (C) 1998 Wiley-Liss, Inc.dagger

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/07/20 alle ore 04:34:28