Hypoxia as an off switch for gene expression

Hypoxia as an off switch for gene expression

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Access through your institution Buy or subscribe DNA hypermethylation at promoters, which manifests with an increase in the levels of 5-methylcytosine (5mC), results in transcriptional repression. In cancer cells, DNA hypermethylation is often concentrated at the promoters of tumour suppressor genes owing to the impairment of demethylation, which occurs by unknown mechanisms. Thienpont _et al_. now show that oxygen deprivation (hypoxia) promotes DNA hypermethylation by interfering with the activity of ten-eleven translocation methylcytosine dioxygenases (TETs) — enzymes that are involved in DNA demethylation. The first step of 5mC demethylation involves its TET-mediated oxidation to 5-hydroxymethylcytosine (5hmC). As this step involves oxygen, the authors reasoned that hypoxia, which is frequently associated with tumour expansion, might be linked to the impairment of DNA demethylation observed in cancer cells. Indeed, in hypoxic human and murine cell lines, global levels of 5hmC were decreased and this was linked to decreased TET activity resulting from hypoxia. The loss of 5hmC in hypoxic cells was most prevalent at promoter regions and it was associated with a concomitant increase in the levels of 5mC and a decrease in gene expression from the affected loci. Thus, hypoxia-induced impairment of TET activity directly translates to DNA hypermethylation with functional consequences for gene expression. Importantly, 5hmC levels were also decreased in cells from hypoxic regions of human tumours, which suggests that hypoxia drives DNA hypermethylation in cancers _in vivo_. This is a preview of subscription content, access via your institution ACCESS OPTIONS Access through your institution Subscribe to this journal Receive 12 print issues and online access $209.00 per year only $17.42 per issue Learn more Buy this article * Purchase on SpringerLink * Instant access to full article PDF Buy now Prices may be subject to local taxes which are calculated during checkout ADDITIONAL ACCESS OPTIONS: * Log in * Learn about institutional subscriptions * Read our FAQs * Contact customer support REFERENCES * Thienpont, B. et al. Tumour hypoxia causes DNA hypermethylation by reducing TET activity. _Nature_ http://dx.doi.org/10.1038/nature19081 (2016) Download references Authors * Paulina Strzyz View author publications You can also search for this author inPubMed Google Scholar RELATED LINKS RELATED LINKS RELATED LINKS IN NATURE RESEARCH Pastor, W. A., Aravind, L. & Rao, A. TETonic shift: biological roles of TET proteins in DNA demethylation and transcription. _Nat. Rev. Mol. Cell Biol._ 14, 341–356 (2013) RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Strzyz, P. Hypoxia as an off switch for gene expression. _Nat Rev Mol Cell Biol_ 17, 610 (2016). https://doi.org/10.1038/nrm.2016.119 Download citation * Published: 01 September 2016 * Issue Date: October 2016 * DOI: https://doi.org/10.1038/nrm.2016.119 SHARE THIS ARTICLE Anyone you share the following link with will be able to read this content: Get shareable link Sorry, a shareable link is not currently available for this article. Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative

Access through your institution Buy or subscribe DNA hypermethylation at promoters, which manifests with an increase in the levels of 5-methylcytosine (5mC), results in transcriptional


repression. In cancer cells, DNA hypermethylation is often concentrated at the promoters of tumour suppressor genes owing to the impairment of demethylation, which occurs by unknown


mechanisms. Thienpont _et al_. now show that oxygen deprivation (hypoxia) promotes DNA hypermethylation by interfering with the activity of ten-eleven translocation methylcytosine


dioxygenases (TETs) — enzymes that are involved in DNA demethylation. The first step of 5mC demethylation involves its TET-mediated oxidation to 5-hydroxymethylcytosine (5hmC). As this step


involves oxygen, the authors reasoned that hypoxia, which is frequently associated with tumour expansion, might be linked to the impairment of DNA demethylation observed in cancer cells.


Indeed, in hypoxic human and murine cell lines, global levels of 5hmC were decreased and this was linked to decreased TET activity resulting from hypoxia. The loss of 5hmC in hypoxic cells


was most prevalent at promoter regions and it was associated with a concomitant increase in the levels of 5mC and a decrease in gene expression from the affected loci. Thus, hypoxia-induced


impairment of TET activity directly translates to DNA hypermethylation with functional consequences for gene expression. Importantly, 5hmC levels were also decreased in cells from hypoxic


regions of human tumours, which suggests that hypoxia drives DNA hypermethylation in cancers _in vivo_. This is a preview of subscription content, access via your institution ACCESS OPTIONS


Access through your institution Subscribe to this journal Receive 12 print issues and online access $209.00 per year only $17.42 per issue Learn more Buy this article * Purchase on


SpringerLink * Instant access to full article PDF Buy now Prices may be subject to local taxes which are calculated during checkout ADDITIONAL ACCESS OPTIONS: * Log in * Learn about


institutional subscriptions * Read our FAQs * Contact customer support REFERENCES * Thienpont, B. et al. Tumour hypoxia causes DNA hypermethylation by reducing TET activity. _Nature_


http://dx.doi.org/10.1038/nature19081 (2016) Download references Authors * Paulina Strzyz View author publications You can also search for this author inPubMed Google Scholar RELATED LINKS


RELATED LINKS RELATED LINKS IN NATURE RESEARCH Pastor, W. A., Aravind, L. & Rao, A. TETonic shift: biological roles of TET proteins in DNA demethylation and transcription. _Nat. Rev.


Mol. Cell Biol._ 14, 341–356 (2013) RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Strzyz, P. Hypoxia as an off switch for gene expression. _Nat Rev Mol


Cell Biol_ 17, 610 (2016). https://doi.org/10.1038/nrm.2016.119 Download citation * Published: 01 September 2016 * Issue Date: October 2016 * DOI: https://doi.org/10.1038/nrm.2016.119 SHARE


THIS ARTICLE Anyone you share the following link with will be able to read this content: Get shareable link Sorry, a shareable link is not currently available for this article. Copy to


clipboard Provided by the Springer Nature SharedIt content-sharing initiative