c-Met signaling in the development of tumorigenesis and chemoresistance: potential applications in pancreatic cancer

Daniel Delitto; Eva Vertes-George; Steven J Hughes; Kevin E Behrns; Jose G Trevino

doi:10.3748/wjg.v20.i26.8458

c-Met signaling in the development of tumorigenesis and chemoresistance: potential applications in pancreatic cancer

World J Gastroenterol. 2014 Jul 14;20(26):8458-70. doi: 10.3748/wjg.v20.i26.8458.

Authors

Daniel Delitto¹, Eva Vertes-George¹, Steven J Hughes¹, Kevin E Behrns¹, Jose G Trevino¹

Affiliation

¹ Daniel Delitto, Steven J Hughes, Kevin E Behrns, Jose G Trevino, Department of Surgery, University of Florida-Gainesville, Gainesville, FL 32610, United States.

Abstract

Pancreatic ductal adenocarcinoma is the 4(th) leading cause of cancer deaths in the United States. The majority of patients are candidates only for palliative chemotherapy, which has proven largely ineffective in halting tumor progression. One proposed mechanism of chemoresistance involves signaling via the mesenchymal-epithelial transition factor protein (MET), a previously established pathway critical to cell proliferation and migration. Here, we review the literature to characterize the role of MET in the development of tumorigenesis, metastasis and chemoresistance, highlighting the potential of MET as a therapeutic target in pancreatic cancer. In this review, we characterize the role of c-Met in the development of tumorigenesis, metastasis and chemoresistance, highlighting the potential of c-Met as a therapeutic target in pancreatic cancer.

Keywords: Chemoresistance; Pancreatic adenocarcinoma; Receptor tyrosine kinase; c-Met.

Publication types

Review

MeSH terms

Animals
Antineoplastic Agents / therapeutic use
Biomarkers, Tumor / antagonists & inhibitors
Biomarkers, Tumor / genetics
Biomarkers, Tumor / metabolism*
Carcinoma, Pancreatic Ductal / drug therapy
Carcinoma, Pancreatic Ductal / enzymology*
Carcinoma, Pancreatic Ductal / genetics
Carcinoma, Pancreatic Ductal / secondary
Cell Transformation, Neoplastic / genetics
Cell Transformation, Neoplastic / metabolism*
Cell Transformation, Neoplastic / pathology
Drug Design
Drug Resistance, Neoplasm* / genetics
Humans
Molecular Targeted Therapy
Neoplastic Stem Cells / enzymology
Pancreatic Neoplasms / drug therapy
Pancreatic Neoplasms / enzymology*
Pancreatic Neoplasms / genetics
Pancreatic Neoplasms / pathology
Protein Kinase Inhibitors / therapeutic use
Proto-Oncogene Proteins c-met / antagonists & inhibitors
Proto-Oncogene Proteins c-met / genetics
Proto-Oncogene Proteins c-met / metabolism*
Signal Transduction / drug effects*

Substances

Antineoplastic Agents
Biomarkers, Tumor
Protein Kinase Inhibitors
Proto-Oncogene Proteins c-met