The RON receptor tyrosine kinase in pancreatic cancer pathogenesis and its potential implications for future targeted therapies

Pancreas. 2014 Mar;43(2):183-9. doi: 10.1097/MPA.0000000000000088.

Abstract

Pancreatic cancer remains a devastating disease with a mortality rate that has not changed substantially in decades. Novel therapies are therefore desperately needed. The RON receptor tyrosine kinase has been identified as an important mediator of KRAS oncogene addiction and is overexpressed in the majority of pancreatic cancers. Preclinical studies show that inhibition of RON function decreases pancreatic cancer cell migration, invasion, and survival and can sensitize pancreatic cancer cells to chemotherapy. This article reviews the current state of knowledge regarding RON biology and pancreatic cancer and discusses its potential as a therapeutic target.

Publication types

  • Review

MeSH terms

  • Antibodies, Monoclonal / therapeutic use*
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Proliferation / drug effects
  • Forecasting
  • Humans
  • Molecular Targeted Therapy / methods*
  • Molecular Targeted Therapy / trends
  • Pancreatic Neoplasms / drug therapy*
  • Pancreatic Neoplasms / metabolism
  • Pancreatic Neoplasms / pathology
  • Receptor Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Receptor Protein-Tyrosine Kinases / immunology
  • Receptor Protein-Tyrosine Kinases / metabolism
  • Signal Transduction / drug effects

Substances

  • Antibodies, Monoclonal
  • RON protein
  • Receptor Protein-Tyrosine Kinases