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2015 ; 2015
(ä): 198967
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Epithelial Plasticity in Cancer: Unmasking a MicroRNA Network for TGF-?-, Notch-,
and Wnt-Mediated EMT
#MMPMID25883651
Zoni E
; van der Pluijm G
; Gray PC
; Kruithof-de Julio M
J Oncol
2015[]; 2015
(ä): 198967
PMID25883651
show ga
Epithelial-to-mesenchymal transition (EMT) is a reversible process by which
cancer cells can switch from a sessile epithelial phenotype to an invasive
mesenchymal state. EMT enables tumor cells to become invasive, intravasate,
survive in the circulation, extravasate, and colonize distant sites. Paracrine
heterotypic stroma-derived signals as well as paracrine homotypic or autocrine
signals can mediate oncogenic EMT and contribute to the acquisition of
stem/progenitor cell properties, expansion of cancer stem cells, development of
therapy resistance, and often lethal metastatic disease. EMT is regulated by a
variety of stimuli that trigger specific intracellular signalling pathways.
Altered microRNA (miR) expression and perturbed signalling pathways have been
associated with epithelial plasticity, including oncogenic EMT. In this review we
analyse and describe the interaction between experimentally validated miRs and
their target genes in TGF-?, Notch, and Wnt signalling pathways. Interestingly,
in this process, we identified a "signature" of 30 experimentally validated miRs
and a cluster of validated target genes that seem to mediate the cross talk
between TGF-?, Notch, and Wnt signalling networks during EMT and reinforce their
connection to the regulation of epithelial plasticity in health and disease.