Curcumin enhances cytotoxicity of chemotherapeutic agents in prostate cancer cells by inducing p21(WAF1/CIP1) and C/EBPbeta expressions and suppressing NF-kappaB activation

Prostate. 2002 May 15;51(3):211-8. doi: 10.1002/pros.10089.

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 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / therapeutic use*
  • CCAAT-Enhancer-Binding Protein-beta / metabolism*
  • Cell Cycle / drug effects
  • Cell Nucleus / metabolism
  • Curcumin / pharmacology*
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins / metabolism*
  • DNA / metabolism
  • Drug Synergism
  • Humans
  • Male
  • NF-kappa B / antagonists & inhibitors*
  • NF-kappa B / metabolism
  • Pregnancy-Specific beta 1-Glycoproteins
  • Prostatic Neoplasms / drug therapy*
  • Prostatic Neoplasms / metabolism
  • Prostatic Neoplasms / pathology
  • Sp1 Transcription Factor / metabolism
  • Tumor Cells, Cultured
  • Up-Regulation

Substances

  • Antineoplastic Agents
  • CCAAT-Enhancer-Binding Protein-beta
  • CDKN1A protein, human
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • NF-kappa B
  • Pregnancy-Specific beta 1-Glycoproteins
  • Sp1 Transcription Factor
  • DNA
  • Curcumin