Skip to main content
padlock icon - secure page this page is secure

Hypoxia induces the expression of TET enzymes in HepG2 cells

Buy Article:

$42.00 + tax (Refund Policy)

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 teneleventranslocation 5methylcytosine dioxygenase (TET) enzymes, which catalyze the conversion of 5methylcytosine to 5hydroxymethylcytosine (5hmC), thereby leading to elevated cellular 5hmC levels in hepatoblastoma HepG2 cells. Hypoxia inducible factor1α (HIF1α) is the main transcription factor activated by hypoxia. A chemical inducer of HIF1α, CoCl2, also increases the expression of TET enzymes. Knockdown of HIF1α attenuates the hypoxiainduced expression of TET enzymes. These results indicate that hypoxia controls DNA methylation through HIF1αmediated TET enzyme regulation in HepG2 cells.
No Reference information available - sign in for access.
No Citation information available - sign in for access.
No Supplementary Data.
No Article Media
No Metrics

Document Type: Research Article

Affiliations: Department of the First General Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning 110032, P.R. China

Publication date: January 1, 2017

More about this publication?
  • Oncology Letters is a monthly, peer-reviewed journal, available in print and online, that focuses on all aspects of clinical oncology, as well as in vitro and in vivo experimental model systems relevant to the mechanisms of disease.

    The principal aim of Oncology Letters is to provide the prompt publication of original studies of high quality that pertain to clinical oncology, chemotherapy, oncogenes, carcinogenesis, metastasis, epidemiology and viral oncology in the form of original research, reviews and case reports.
  • Editorial Board
  • Information for Authors
  • Submit a Paper
  • Subscribe to this Title
  • Information for Advertisers
  • Terms & Conditions
  • Ingenta Connect is not responsible for the content or availability of external websites
  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more