Fluoxetine synergys with anticancer drugs to overcome multidrug resistance in breast cancer cells

Tumour Biol. 2012 Oct;33(5):1299-306. doi: 10.1007/s13277-012-0377-4. Epub 2012 May 2.

Abstract

Multidrug resistance (MDR) is the main obstacle in breast cancer chemotherapy, a reversal reagent with high reversal effect but low toxicity is the hotpot issue at present. The antidepressant fluoxetine (FLX) is a new highly effective chemosensitizer; however, the possible mechanism of FLX in reversal of MDR is unclear. In this study, the effect of FLX on MDR mediated by apoptosis was researched in resistant/sensitive breast cancer cells, which treated by FLX/adriamycin (ADM)/paclitaxel (PTX) alone or FLX-ADM, FLX-PTX combination. Apoptosis assay demonstrated that FLX combined with ADM enhanced the proportion of apoptosis remarkably in MCF-7/ADM but not MCF-7 cells; however, increased the apoptosis rates in both cells when FLX-PTX combination. Results of apoptosis proteins assay showed a upgrade of p53 and a downgrade of Bcl-2 level by FLX-ADM or FLX-PTX combinations in both cells. Our findings indicated that by synergism with anticancer drugs, FLX modulation of apoptosis via targeting p53 and Bcl-2 expression, FLX reverse the breast cancer cell's resistance and enhance the chemosensitivity to ADM and PTX.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Combined Chemotherapy Protocols / pharmacology*
  • Apoptosis / drug effects
  • Breast Neoplasms / drug therapy
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism*
  • Cell Proliferation / drug effects
  • Drug Resistance, Multiple
  • Drug Resistance, Neoplasm* / genetics
  • Drug Synergism
  • Female
  • Fluoxetine / administration & dosage
  • Fluoxetine / pharmacology*
  • Gene Expression Regulation, Neoplastic
  • Humans
  • MCF-7 Cells
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Selective Serotonin Reuptake Inhibitors / administration & dosage
  • Selective Serotonin Reuptake Inhibitors / pharmacology*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Proto-Oncogene Proteins c-bcl-2
  • Serotonin Uptake Inhibitors
  • Tumor Suppressor Protein p53
  • Fluoxetine