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2016 ; 5
(2
): ä Nephropedia Template TP
gab.com Text
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English Wikipedia
Hypoxia, Epithelial-Mesenchymal Transition, and TET-Mediated Epigenetic Changes
#MMPMID26861406
Kao SH
; Wu KJ
; Lee WH
J Clin Med
2016[Feb]; 5
(2
): ä PMID26861406
show ga
Tumor hypoxia is a pathophysiologic outcome of disrupted microcirculation with
inadequate supply of oxygen, leading to enhanced proliferation,
epithelial-mesenchymal transition (EMT), metastasis, and chemo-resistance.
Epigenetic changes induced by hypoxia are well documented, and they lead to tumor
progression. Recent advances show that DNA demethylation mediated by the
Ten-eleven translocation (TET) proteins induces major epigenetic changes and
controls key steps of cancer development. TET enzymes serve as 5mC
(5-methylcytosine)-specific dioxygenases and cause DNA demethylation. Hypoxia
activates the expression of TET1, which also serves as a co-activator of HIF-1?
transcriptional regulation to modulate HIF-1? downstream target genes and promote
epithelial-mesenchymal transition. As HIF is a negative prognostic factor for
tumor progression, hypoxia-activated prodrugs (HAPs) may provide a favorable
therapeutic approach to lessen hypoxia-induced malignancy.