REIC/Dkk-3 overexpression downregulates P-glycoprotein in multidrug-resistant MCF7/ADR cells and induces apoptosis in breast cancer

Cancer Gene Ther. 2009 Jan;16(1):65-72. doi: 10.1038/cgt.2008.58. Epub 2008 Jul 25.

Abstract

The overexpression of reduced expression in immortalized cells (REIC)/Dickkopf-3 (Dkk-3), a tumor suppressor gene, induced apoptosis in human prostatic and testicular cancer cells. The aim of this study is to examine the potential of REIC/Dkk-3 as a therapeutic target against breast cancer. First, the in vitro apoptotic effect of Ad-REIC treatment was investigated in breast cancer cell lines and the adenovirus-mediated overexpression of REIC/Dkk-3 was thus found to lead to apoptotic cell death in a c-Jun-NH(2)-kinase (JNK) phosphorylaion-dependent manner. Moreover, an in vivo apoptotic effect and MCF/Wt tumor growth inhibition were observed in the mouse model after intratumoral Ad-REIC injection. As multidrug resistance (MDR) is a major problem in the chemotherapy of progressive breast cancer, the in vitro effects of Ad-REIC treatment were investigated in terms of the sensitivity of multidrug-resistant MCF7/ADR cells to doxorubicin and of the P-glycoprotein expression. Ad-REIC treatment in MCF7/ADR cells also downregulated P-glycoprotein expresssion through JNK activation, and sensitized its drug resistance against doxorubicin. Therefore, not only apoptosis induction but also the reversal of anticancer drug resistance was achieved using Ad-REIC. We suggest that REIC/Dkk-3 is a novel target for breast cancer treatment and that Ad-REIC might be an attractive agent against drug-resistant cancer in combination with conventional antineoplastic agents.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B, Member 1 / biosynthesis*
  • ATP Binding Cassette Transporter, Subfamily B, Member 1 / genetics
  • Adaptor Proteins, Signal Transducing
  • Adenoviridae*
  • Animals
  • Antibiotics, Antineoplastic / pharmacology*
  • Antibiotics, Antineoplastic / therapeutic use
  • Apoptosis* / drug effects
  • Apoptosis* / genetics
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / therapy*
  • Chemokines
  • Down-Regulation* / drug effects
  • Down-Regulation* / genetics
  • Doxorubicin / pharmacology*
  • Doxorubicin / therapeutic use
  • Drug Resistance, Multiple* / drug effects
  • Drug Resistance, Multiple* / genetics
  • Drug Resistance, Neoplasm* / drug effects
  • Drug Resistance, Neoplasm* / genetics
  • Enzyme Activation / drug effects
  • Enzyme Activation / genetics
  • Female
  • Genetic Therapy*
  • HeLa Cells
  • Humans
  • Intercellular Signaling Peptides and Proteins / biosynthesis*
  • Intercellular Signaling Peptides and Proteins / genetics
  • MAP Kinase Kinase 4 / genetics
  • MAP Kinase Kinase 4 / metabolism
  • Mice
  • Mice, Nude
  • Neoplasm Transplantation

Substances

  • ATP Binding Cassette Transporter, Subfamily B, Member 1
  • Adaptor Proteins, Signal Transducing
  • Antibiotics, Antineoplastic
  • Chemokines
  • DKK3 protein, human
  • Intercellular Signaling Peptides and Proteins
  • Doxorubicin
  • MAP Kinase Kinase 4