Targeting C-Met in Cancer by Micrornas: Potential Therapeutic Applications in Hepatocellular Carcinoma
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Date
2015-09-12
Authors
Journal Title
Journal ISSN
Volume Title
Publisher
Wiley-Liss Inc.
Open Access Color
Green Open Access
Yes
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Publicly Funded
No
Abstract
Preclinical Research Cancer is one of the world's deadliest diseases, with very low survival rates and increased occurrence in the future. Successfully developed target-based therapies have significantly changed cancer treatment. However, primary and/or acquired resistance in the tumor is a major challenge in current therapies and novel combinational therapies are required. RNA interference-mediated gene inactivation, alone or in combination with other current therapies, provides novel promising therapeutics that can improve cure rate and overcome resistance mechanisms to conventional therapeutics. Hepatocyte Growth Factor/c-Met signaling is one of the most frequently dysregulated pathways in human cancers and abnormal c-Met activation is correlated with poor clinical outcomes and drug resistance in hepatocellular carcinoma (HCC). In recent years, a growing number of studies have identified several inhibitors and microRNAs (miRNAs), specifically targeting c-Met in various cancers, including HCC. In this review, we discuss current knowledge regarding miRNAs, focusing on their involvement in cancer and their potential as research tools and therapeutics. Then, we focus on the potential use of c-Met targeting miRNAs for suppressing aberrant c-Met signaling in HCC treatment. Drug Dev Res 76: 357-367, 2015. © 2015 Wiley Periodicals, Inc. © 2015 Wiley Periodicals, Inc.
Description
Keywords
c-Met, hepatocellular carcinoma, hepatocyte growth factor, miRNA, targeted therapy, microRNA, microRNA 122, microRNA 148a, microRNA 181a 5p, microRNA 199a 3p, microRNA 26a, microRNA 34, microRNA 93, scatter factor, scatter factor receptor, unclassified drug, microRNA, scatter factor receptor, 3' untranslated region, angiogenesis, antiangiogenic activity, apoptosis, autophosphorylation, binding affinity, cancer inhibition, cell cycle arrest, cell invasion, cell migration, cell motility, cell proliferation, dimerization, drug mechanism, human, liver carcinogenesis, liver cell carcinoma, molecular docking, nonhuman, protein phosphorylation, protein targeting, Review, senescence, signal transduction, antagonists and inhibitors, Carcinoma, Hepatocellular, drug effects, drug resistance, genetics, Liver Neoplasms, metabolism, molecularly targeted therapy, procedures, Carcinoma, Hepatocellular, Drug Resistance, Neoplasm, Humans, Liver Neoplasms, MicroRNAs, Molecular Targeted Therapy, Proto-Oncogene Proteins c-met, MicroRNAs, Carcinoma, Hepatocellular, Drug Resistance, Neoplasm, Liver Neoplasms, Humans, Molecular Targeted Therapy, Proto-Oncogene Proteins c-met
Fields of Science
0301 basic medicine, 0303 health sciences, 03 medical and health sciences
Citation
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Scopus Q
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OpenCitations Citation Count
22
Source
Drug Development Research
Volume
76
Issue
7
Start Page
357
End Page
367
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Citations
CrossRef : 23
Scopus : 25
PubMed : 12
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Mendeley Readers : 20
SCOPUS™ Citations
25
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Page Views
2
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