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  4. Curcumin enhances cytotoxicity of chemotherapeutic agents in prostate cancer cells by inducing p21WAF1/CIP1 and C/EBPβ expressions and suppressing NF-κB activation
 
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Curcumin enhances cytotoxicity of chemotherapeutic agents in prostate cancer cells by inducing p21WAF1/CIP1 and C/EBPβ expressions and suppressing NF-κB activation

Journal
Prostate
Journal Volume
51
Journal Issue
3
Pages
211-218
Date Issued
2002
Author(s)
Hour T.-C.
Chen J.
CHAO-YUAN HUANG  
Guan J.-Y.
Lu S.-H.
YEONG-SHIAU PU  
DOI
10.1002/pros.10089
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-0037093926&doi=10.1002%2fpros.10089&partnerID=40&md5=6ba02b6173458d5ea3cee3b7d4e8ad88
https://scholars.lib.ntu.edu.tw/handle/123456789/544512
Abstract
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 p21WAF1/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. ? 2002 Wiley-Liss, Inc.
SDGs

[SDGs]SDG3

Other Subjects
curcumin; doxorubicin; fluorouracil; immunoglobulin enhancer binding protein; paclitaxel; protein p21; protein p53; animal cell; antineoplastic activity; article; cancer combination chemotherapy; cell cycle; cytotoxicity; drug effect; drug potentiation; nonhuman; priority journal; prostate cancer; transcription initiation; Antineoplastic Agents; CCAAT-Enhancer-Binding Protein-beta; Cell Cycle; Cell Nucleus; Curcumin; Cyclin-Dependent Kinase Inhibitor p21; Cyclins; DNA; Drug Synergism; Humans; Male; NF-kappa B; Pregnancy-Specific beta 1-Glycoproteins; Prostatic Neoplasms; Sp1 Transcription Factor; Tumor Cells, Cultured; Up-Regulation
Type
journal article

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