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Review
. 2017 Jan;5(1):5.
doi: 10.21037/atm.2016.12.67.

MET: roles in epithelial-mesenchymal transition and cancer stemness

Hye-Min Jeon  1 , Jeongwu Lee  1
Affiliations
Review

MET: roles in epithelial-mesenchymal transition and cancer stemness

Hye-Min Jeon et al. Ann Transl Med. 2017 Jan.

Abstract

In a number of cancers, deregulated MET pathway leads to aberrantly activated proliferative and invasive signaling programs that promote malignant transformation, cell motility and migration, angiogenesis, survival in hypoxia, and invasion. A better understanding of oncogenic MET signaling will help us to discover effective therapeutic approaches and to identify which tumors are likely to respond to MET-targeted cancer therapy. In this review, we will summarize the roles of MET signaling in cancer, with particular focus on epithelial-mesenchymal transition (EMT) and cancer stemness. Then, we will provide update on MET targeting agents and discuss the challenges that should be overcome for the development of an effective therapy.

Keywords: MET; cancer stem cell (CSC); epithelial-mesenchymal transition (EMT).

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Conflict of interest statement

The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
MET signaling in cancer. (I) MET signaling is deregulated in cancer through genomic amplification, fusion, and activating mutations, high expression of HGFR and/or HGF, and cross activation with other receptors; (II) activation of MET signaling induces proliferation and survival, migration, invasion and metastasis, angiogenesis and stromal cell communication, cancer stem cell traits, therapeutic resistance and EMT; (III) therapeutic targeting of HGF/MET signaling pathway has been developed and tested in clinical trials, such as, MET blocking antibodies (MetMAB), and small molecule inhibitors (crizotinib, cabozantinib, foretinib, tivantinib). HGF, hepatocyte growth factor; EMT, epithelial-mesenchymal transition.
See this image and copyright information in PMC

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