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c-Met and miRs in Cancer

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. Recen...

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Detalles Bibliográficos
Autores principales: Giglio, Simona, Vecchione, Andrea
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5344231/
https://www.ncbi.nlm.nih.gov/pubmed/28536397
http://dx.doi.org/10.3390/biomedicines3010032
Descripción
Sumario: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.