FAK and Paxillin, Two Potential Targets in Pancreatic Cancer

Oncotarget. 2016 May 24;7(21):31586-601. doi: 10.18632/oncotarget.8040.

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a devastating cancer in large part due to late diagnosis and a lack of effective screening tests. In spite of recent progress in imaging, surgery and new therapeutic options for pancreatic cancer, the overall five-year survival still remains unacceptably low. Numerous studies have shown that focal adhesion kinase (FAK) is activated in many cancers including PDAC and promotes cancer progression and metastasis. Paxillin, an intracellular adaptor protein that plays a key role in cytoskeletal organization, connects integrins to FAK and plays a key role in assembly and disassembly of focal adhesions. Here, we have reviewed evidence in support of FAK as a potential therapeutic target and summarized related combinatorial therapies.

Keywords: FAK; P53; integrins; pancreatic cancer; paxillin.

Publication types

  • Review

MeSH terms

  • Biomarkers, Tumor / antagonists & inhibitors
  • Biomarkers, Tumor / metabolism
  • Carcinoma, Pancreatic Ductal / drug therapy
  • Carcinoma, Pancreatic Ductal / metabolism*
  • Carcinoma, Pancreatic Ductal / pathology
  • Focal Adhesion Kinase 1 / antagonists & inhibitors
  • Focal Adhesion Kinase 1 / metabolism*
  • Humans
  • Models, Biological
  • Molecular Targeted Therapy / methods
  • Pancreatic Neoplasms / drug therapy
  • Pancreatic Neoplasms / metabolism*
  • Pancreatic Neoplasms / pathology
  • Paxillin / antagonists & inhibitors
  • Paxillin / metabolism*
  • Protein Kinase Inhibitors / therapeutic use
  • Signal Transduction / drug effects

Substances

  • Biomarkers, Tumor
  • Paxillin
  • Protein Kinase Inhibitors
  • Focal Adhesion Kinase 1
  • PTK2 protein, human