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Cancers 2017, 9(7), 87; https://doi.org/10.3390/cancers9070087

Role and Therapeutic Targeting of the HGF/MET Pathway in Glioblastoma

1
Department of Microbiology, Immunology & Cancer Biology, University of Virginia, Charlottesville, VA 22908, USA
2
Department of Neurology and The Cancer Center, Department of Microbiology, Immunology & Cancer Biology, University of Virginia, Charlottesville, VA 22908, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Jill M. Siegfried
Received: 5 June 2017 / Revised: 29 June 2017 / Accepted: 6 July 2017 / Published: 11 July 2017
(This article belongs to the Special Issue Hepatocyte Growth Factor Pathway in Cancer)
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Abstract

Glioblastoma (GBM) is a lethal brain tumor with dismal prognosis. Current therapeutic options, consisting of surgery, chemotherapy and radiation, have only served to marginally increase patient survival. Receptor tyrosine kinases (RTKs) are dysregulated in approximately 90% of GBM; attributed to this, research has focused on inhibiting RTKs as a novel and effective therapy for GBM. Overexpression of RTK mesenchymal epithelial transition (MET), and its ligand, hepatocyte growth factor (HGF), in GBM highlights a promising new therapeutic target. This review will discuss the role of MET in cell cycle regulation, cell proliferation, evasion of apoptosis, cell migration and invasion, angiogenesis and therapeutic resistance in GBM. It will also discuss the modes of deregulation of HGF/MET and their regulation by microRNAs. As the HGF/MET pathway is a vital regulator of multiple pro-survival pathways, efforts and strategies for its exploitation for GBM therapy are also described. View Full-Text
Keywords: Glioblastoma; HGF; MET Glioblastoma; HGF; MET
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Cruickshanks, N.; Zhang, Y.; Yuan, F.; Pahuski, M.; Gibert, M.; Abounader, R. Role and Therapeutic Targeting of the HGF/MET Pathway in Glioblastoma. Cancers 2017, 9, 87.

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