Journal
ONCOLOGY LETTERS
Volume 14, Issue 6, Pages 6457-6462Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2017.7063
Keywords
hypoxia; ten-eleven-translocation 5-methylcytosine dioxygenase; hypoxia inducible factor-1 alpha; 5-hydroxymethylcytosine; methylation
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Hypoxia promotes tumor malignancy in solid tumors. One key mechanism by which this occurs is via epigenetic alteration. The present study demonstrates that hypoxia upregulates the expression of the ten-eleven-translocation 5-methylcytosine dioxygenase (TET) enzymes, which catalyze the conversion of 5-methylcytosine to 5-hydroxymethylcytosine (5-hmC), thereby leading to elevated cellular 5-hmC levels in hepatoblastoma HepG2 cells. Hypoxia inducible factor-1 alpha (HIF-1 alpha) is the main transcription factor activated by hypoxia. A chemical inducer of HIF-1 alpha, CoCl2, also increases the expression of TET enzymes. Knockdown of HIF-1 alpha attenuates the hypoxia-induced expression of TET enzymes. These results indicate that hypoxia controls DNA methylation through HIF-1 alpha-mediated TET enzyme regulation in HepG2 cells.
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