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Biomedicines 2015, 3(1), 32-44; doi:10.3390/biomedicines3010032

c-Met and miRs in Cancer

Department of Clinical and Molecular Medicine, Sapienza University of Rome, Rome 00161, Italy
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Academic Editor: Kenneth Cornetta
Received: 29 September 2014 / Accepted: 24 December 2014 / Published: 5 January 2015
(This article belongs to the Special Issue New aspects of the Hepatocyte Growth Factor/c-Met System)
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Abstract

c-Met, a member of the receptor tyrosine kinase family, is involved in a wide range of cellular processes, including tumor survival, cell growth, angiogenesis and metastasis, and resulting in overexpression in many human cancers, leading to a constitutive activation of the downstream pathways. Recently identified MicroRNAs are a family of small noncoding RNA molecules, extensively studied in cancer, that exert their action by inhibiting gene expression at the posttranscriptional level in several biological processes. Aberrant regulation of microRNAs expression has been implicated in the pathogenesis of different human neoplasia. Several publications point out the connections between c-Met and its ligand hepatocyte growth factor (HGF) and microRNAs. This review summarizes the current knowledge about the interplay between c-Met/HGF and microRNAs and provides evidence that microRNAs are a novel and additional system to regulate c-Met expression in tumors. In the future, microRNAs connected to c-Met may provide an additional option to inhibiting this oncogene from orchestrating an invasive growth program. View Full-Text
Keywords: microRNA; c-MET; HGF; cancer microRNA; c-MET; HGF; cancer
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Giglio, S.; Vecchione, A. c-Met and miRs in Cancer. Biomedicines 2015, 3, 32-44.

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