Format

Send to

Choose Destination
BMB Rep. 2019 Apr;52(4):239-249.

Proteolytic cleavages of MET: the divide-and-conquer strategy of a receptor tyrosine kinase.

Author information

1
University of Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T - Mechanisms of Tumorigenesis and Target Therapies, F-59000 Lille, France.

Abstract

Membrane-anchored full-length MET stimulated by its ligand HGF/SF induces various biological responses, including survival, growth, and invasion. This panel of responses, referred to invasive growth, is required for embryogenesis and tissue regeneration in adults. On the contrary, MET deregulation is associated with tumorigenesis in many kinds of cancer. In addition to its well-documented ligand-stimulated downstream signaling, the receptor can be cleaved by proteases such as secretases, caspases, and calpains. These cleavages are involved either in MET receptor inactivation or, more interestingly, in generating active fragments that can modify cell fate. For instance, MET fragments can promote cell death or invasion. Given a large number of proteases capable of cleaving MET, this receptor appears as a prototype of proteolytic-cleavage-regulated receptor tyrosine kinase. In this review, we describe and discuss the mechanisms and consequences, both physiological and pathological, of MET proteolytic cleavages. [BMB Reports 2019; 52(4): 239-249].

PMID:
30670153
PMCID:
PMC6507848

Supplemental Content

Full text links

Icon for Korean Society for Biochemistry and Molecular Biology Icon for PubMed Central
Loading ...
Support Center