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10.3390/jcm5020024

http://scihub22266oqcxt.onion/10.3390/jcm5020024
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C4773780!4773780!26861406
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suck abstract from ncbi


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pmid26861406      J+Clin+Med 2016 ; 5 (2): ä
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  • Hypoxia, Epithelial-Mesenchymal Transition, and TET-Mediated Epigenetic Changes #MMPMID26861406
  • Kao SH; Wu KJ; Lee WH
  • J Clin Med 2016[Feb]; 5 (2): ä PMID26861406show 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.
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