Blockade of PAR1 signaling with cell-penetrating pepducins inhibits Akt survival pathways in breast cancer cells and suppresses tumor survival and metastasis

Cancer Res. 2009 Aug 1;69(15):6223-31. doi: 10.1158/0008-5472.CAN-09-0187. Epub 2009 Jul 21.

Abstract

Protease-activated receptor 1 (PAR1) is a G protein-coupled receptor that is not expressed in normal breast epithelia but is up-regulated in invasive breast carcinomas. In the present study, we found that matrix metalloprotease-1 (MMP-1) robustly activates the PAR1-Akt survival pathway in breast carcinoma cells. This process is blocked by a cell-penetrating lipopeptide "pepducin," P1pal-7, which is a potent inhibitor of cell viability in breast carcinoma cells expressing PAR1. Both a MMP-1 inhibitor and P1pal-7 significantly promote apoptosis in breast tumor xenografts and inhibit metastasis to the lungs by up to 88%. Dual therapy with P1pal-7 and Taxotere inhibits the growth of MDA-MB-231 xenografts by 95%. Consistently, biochemical analysis of xenograft tumors treated with P1pal-7 or MMP-1 inhibitor showed attenuated Akt activity. Ectopic expression of constitutively active Akt rescues breast cancer cells from the synergistic cytotoxicity of P1pal-7 and Taxotere, suggesting that Akt is a critical component of PAR1-dependent cancer cell viability. Together, these findings indicate that blockade of MMP1-PAR1 signaling may provide a benefit beyond treatment with Taxotere alone in advanced, metastatic breast cancer.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Combined Chemotherapy Protocols / administration & dosage
  • Apoptosis / drug effects
  • Breast Neoplasms / drug therapy*
  • Breast Neoplasms / enzymology
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Caspases / metabolism
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Cell Survival / physiology
  • Docetaxel
  • Drug Synergism
  • Enzyme Activation
  • Female
  • Humans
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / secondary
  • Matrix Metalloproteinase 1 / metabolism
  • Matrix Metalloproteinase Inhibitors
  • Mice
  • Mice, Nude
  • Peptides / administration & dosage
  • Peptides / pharmacokinetics
  • Peptides / pharmacology*
  • Proto-Oncogene Proteins c-akt / antagonists & inhibitors*
  • Proto-Oncogene Proteins c-akt / metabolism
  • RNA, Small Interfering / genetics
  • Receptor, PAR-1 / antagonists & inhibitors*
  • Receptor, PAR-1 / genetics
  • Receptor, PAR-1 / metabolism
  • Signal Transduction / drug effects
  • Taxoids / administration & dosage
  • Xenograft Model Antitumor Assays

Substances

  • Matrix Metalloproteinase Inhibitors
  • Peptides
  • RNA, Small Interfering
  • Receptor, PAR-1
  • Taxoids
  • Docetaxel
  • Proto-Oncogene Proteins c-akt
  • Caspases
  • MMP1 protein, human
  • Matrix Metalloproteinase 1