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Curcumin enhances cytotoxicity of chemotherapeutic agents in prostate cancer cells by inducing p21 WAF1/CIP1 and C/EBPβ expressions and suppressing NF‐κB activation
Author(s) -
Hour TzyhChyuan,
Chen Jun,
Huang ChaoYuan,
Guan JingYi,
Lu ShiuHui,
Pu YeongShiau
Publication year - 2002
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.10089
Subject(s) - cytotoxicity , curcumin , du145 , prostate cancer , flow cytometry , cancer research , pharmacology , prostate , cytotoxic t cell , cell growth , cell cycle , chemistry , cancer , medicine , immunology , lncap , biochemistry , in vitro
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/EBPβ. Moreover, CCM was able to inhibit both the constitutional and TNF‐α‐induced NF‐κB activation in a time‐dependent manner. CONCLUSIONS The incorporation of CCM into cytotoxic therapies may be a promising strategy for the treatment of AIPC. Prostate 51: 211–218, 2002. © 2002 Wiley‐Liss, Inc.