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10.1186/s12943-016-0541-3

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suck abstract from ncbi


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pmid27590724
      Mol+Cancer 2016 ; 15 (1 ): 56
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  • Wnt-signalling pathways and microRNAs network in carcinogenesis: experimental and bioinformatics approaches #MMPMID27590724
  • Onyido EK ; Sweeney E ; Nateri AS
  • Mol Cancer 2016[Sep]; 15 (1 ): 56 PMID27590724 show ga
  • Over the past few years, microRNAs (miRNAs) have not only emerged as integral regulators of gene expression at the post-transcriptional level but also respond to signalling molecules to affect cell function(s). miRNAs crosstalk with a variety of the key cellular signalling networks such as Wnt, transforming growth factor-? and Notch, control stem cell activity in maintaining tissue homeostasis, while if dysregulated contributes to the initiation and progression of cancer. Herein, we overview the molecular mechanism(s) underlying the crosstalk between Wnt-signalling components (canonical and non-canonical) and miRNAs, as well as changes in the miRNA/Wnt-signalling components observed in the different forms of cancer. Furthermore, the fundamental understanding of miRNA-mediated regulation of Wnt-signalling pathway and vice versa has been significantly improved by high-throughput genomics and bioinformatics technologies. Whilst, these approaches have identified a number of specific miRNA(s) that function as oncogenes or tumour suppressors, additional analyses will be necessary to fully unravel the links among conserved cellular signalling pathways and miRNAs and their potential associated components in cancer, thereby creating therapeutic avenues against tumours. Hence, we also discuss the current challenges associated with Wnt-signalling/miRNAs complex and the analysis using the biomedical experimental and bioinformatics approaches.
  • |*Wnt Signaling Pathway [MESH]
  • |Animals [MESH]
  • |Carcinogenesis/*genetics [MESH]
  • |Computational Biology/*methods [MESH]
  • |Gene Expression Profiling [MESH]
  • |Gene Expression Regulation, Neoplastic [MESH]
  • |Gene Regulatory Networks [MESH]
  • |Humans [MESH]


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