Targeting the yin and the yang: combined inhibition of the tyrosine kinase c-Src and the tyrosine phosphatase SHP-2 disrupts pancreatic cancer signaling and biology in vitro and tumor formation in vivo

Pancreas. 2013 Jul;42(5):795-806. doi: 10.1097/MPA.0b013e3182793fd7.

Abstract

Objectives: Although c-Src (Src) has emerged as a potential pancreatic cancer target in preclinical studies, Src inhibitors have not demonstrated a significant therapeutic benefit in clinical trials. The objective of these studies was to examine the effects of combining Src inhibition with inhibition of the protein tyrosine phosphatase SHP-2 in pancreatic cancer cells in vitro and in vivo.

Methods: SHP-2 and Src functions were inhibited by siRNA or small molecule inhibitors. The effects of dual Src/SHP-2 functional inhibition were evaluated by Western blot analysis of downstream signaling pathways; cell biology assays to examine caspase activity, viability, adhesion, migration, and invasion in vitro; and an orthotopic nude mouse model to observe pancreatic tumor formation in vivo.

Results: Dual targeting of Src and SHP-2 induces an additive or supra-additive loss of phosphorylation of Akt and ERK-1/2 and corresponding increases in expression of apoptotic markers, relative to targeting either protein individually. Combinatorial inhibition of Src and SHP-2 significantly reduces viability, adhesion, migration, and invasion of pancreatic cancer cells in vitro and tumor formation in vivo, relative to individual Src/SHP-2 inhibition.

Conclusions: These data suggest that the antitumor effects of Src inhibition in pancreatic cancer may be enhanced through simultaneous inhibition of SHP-2.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use
  • Blotting, Western
  • Cell Line, Tumor
  • Cell Movement / drug effects
  • Cell Movement / genetics
  • Cell Survival / drug effects
  • Cell Survival / genetics
  • Dasatinib
  • Drug Synergism
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Humans
  • Mice
  • Mice, Nude
  • Molecular Targeted Therapy
  • Pancreatic Neoplasms / drug therapy*
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / pathology
  • Phosphorylation / drug effects
  • Protein Kinase Inhibitors / administration & dosage
  • Protein Kinase Inhibitors / pharmacology*
  • Protein Tyrosine Phosphatase, Non-Receptor Type 11 / antagonists & inhibitors*
  • Protein Tyrosine Phosphatase, Non-Receptor Type 11 / genetics
  • Protein Tyrosine Phosphatase, Non-Receptor Type 11 / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Pyrimidines / administration & dosage
  • Pyrimidines / pharmacology
  • RNA Interference
  • Signal Transduction / drug effects*
  • Signal Transduction / genetics
  • Thiazoles / administration & dosage
  • Thiazoles / pharmacology
  • Tumor Burden / drug effects
  • Tumor Burden / genetics
  • Vanadates / administration & dosage
  • Vanadates / pharmacology
  • Xenograft Model Antitumor Assays
  • src-Family Kinases / antagonists & inhibitors*
  • src-Family Kinases / genetics
  • src-Family Kinases / metabolism

Substances

  • Protein Kinase Inhibitors
  • Pyrimidines
  • Thiazoles
  • Vanadates
  • src-Family Kinases
  • Proto-Oncogene Proteins c-akt
  • Extracellular Signal-Regulated MAP Kinases
  • PTPN11 protein, human
  • Protein Tyrosine Phosphatase, Non-Receptor Type 11
  • Dasatinib