Protease-activated receptor-1 drives pancreatic cancer progression and chemoresistance

Int J Cancer. 2014 Nov 15;135(10):2294-304. doi: 10.1002/ijc.28726. Epub 2014 Jun 19.

Abstract

Protease activated receptor (PAR)-1 expression in tumor cells is associated with disease progression and overall survival in a variety of cancers of epithelial origin; however, the importance of PAR-1 in the tumor microenvironment remains unexplored. Utilizing an orthotopic pancreatic cancer model in which tumor cells are PAR-1 positive whereas stromal cells are PAR-1 negative, we show that PAR-1 expression in the microenvironment drives progression and induces chemoresistance of pancreatic cancer. PAR-1 enhances monocyte recruitment into the tumor microenvironment by regulating monocyte migration and fibroblast dependent chemokine production thereby inducing chemoresistance. Overall, our data identify a novel role of PAR-1 in the pancreatic tumor microenvironment and suggest that PAR-1 may be an attractive target to reduce drug resistance in pancreatic cancer.

Keywords: chemoresistance; macrophage; microenvironment; protease activated receptors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antimetabolites, Antineoplastic / pharmacology
  • Cell Movement
  • Cell Proliferation
  • Cell Survival
  • Deoxycytidine / analogs & derivatives*
  • Deoxycytidine / pharmacology
  • Disease Models, Animal
  • Disease Progression
  • Drug Resistance, Neoplasm*
  • Gemcitabine
  • Humans
  • Immunoenzyme Techniques
  • Liver Neoplasms / drug therapy
  • Liver Neoplasms / genetics
  • Liver Neoplasms / secondary*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Neovascularization, Pathologic
  • Pancreatic Neoplasms / drug therapy
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / pathology*
  • Prognosis
  • Receptor, PAR-1 / physiology*
  • Signal Transduction
  • Stromal Cells / metabolism
  • Stromal Cells / pathology*
  • Tumor Cells, Cultured

Substances

  • Antimetabolites, Antineoplastic
  • Receptor, PAR-1
  • Deoxycytidine
  • Gemcitabine