BACKGROUND: The modulatory effects and molecular mechanisms of curcumin (CCM) on the cytotoxicity of chemotherapeutic agents to prostate cancer cells were explored. METHODS: The combined effects of CCM and chemotherapeutic agents were examined by three different administration schedules (one concurrent and two sequential treatments) in two androgen-independent prostate cancer (AIPC) cells (PC-3 and DU145). Alteration of cell cycle progression, protein levels, and transcriptional activation in PC-3 cells were assayed by flow cytometry, Western blotting, and gel shift assay, respectively. RESULTS: The combined effects of CCM --> chemotherapeutic agent schedule showed the greatest synergistic cytotoxicity when compared to the other two schedules in both cells. CCM induced a significant G1 arrest in PC-3, which may be mediated by the induction of p21(WAF1/CIP1) and C/EBPbeta. Moreover, CCM was able to inhibit both the constitutional and TNF-alpha-induced NF-kappaB activation in a time-dependent manner. CONCLUSIONS: The incorporation of CCM into cytotoxic therapies may be a promising strategy for the treatment of AIPC. Copyright 2002 Wiley-Liss, Inc.
BACKGROUND: The modulatory effects and molecular mechanisms of curcumin (CCM) on the cytotoxicity of chemotherapeutic agents to prostate cancer cells were explored. METHODS: The combined effects of CCM and chemotherapeutic agents were examined by three different administration schedules (one concurrent and two sequential treatments) in two androgen-independent prostate cancer (AIPC) cells (PC-3 and DU145). Alteration of cell cycle progression, protein levels, and transcriptional activation in PC-3 cells were assayed by flow cytometry, Western blotting, and gel shift assay, respectively. RESULTS: The combined effects of CCM --> chemotherapeutic agent schedule showed the greatest synergistic cytotoxicity when compared to the other two schedules in both cells. CCM induced a significant G1 arrest in PC-3, which may be mediated by the induction of p21(WAF1/CIP1) and C/EBPbeta. Moreover, CCM was able to inhibit both the constitutional and TNF-alpha-induced NF-kappaB activation in a time-dependent manner. CONCLUSIONS: The incorporation of CCM into cytotoxic therapies may be a promising strategy for the treatment of AIPC. Copyright 2002 Wiley-Liss, Inc.
Authors: Stefan Ambs; Robyn L Prueitt; Ming Yi; Robert S Hudson; Tiffany M Howe; Fabio Petrocca; Tiffany A Wallace; Chang-Gong Liu; Stefano Volinia; George A Calin; Harris G Yfantis; Robert M Stephens; Carlo M Croce Journal: Cancer Res Date: 2008-08-01 Impact factor: 12.701
Authors: Stephanie T Dance-Barnes; Nancy D Kock; Joseph E Moore; Elaine Y Lin; Libyadda J Mosley; Ralph B D'Agostino; Thomas P McCoy; Alan J Townsend; Mark Steven Miller Journal: Carcinogenesis Date: 2009-04-09 Impact factor: 4.944