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The role of TET-mediated DNA hydroxymethylation in prostate cancer

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Date
15/02/2018
Author
Smeets, E.
Lynch, A. G.
Prekovic, S.
Van den Broeck, T.
Moris, L
Helsen, C.
Joniau, S.
Claessens, F.
Massie, C. E.
Keywords
Prostate cancer
Epigenetics
TET
DNA hydroxymethylation
5hmC
RC0254 Neoplasms. Tumors. Oncology (including Cancer)
QH426 Genetics
T-NDAS
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Abstract
Ten-eleven translocation (TET) proteins are recently characterized dioxygenases that regulate demethylation by oxidizing 5-methylcytosine to 5-hydroxymethylcytosine and further derivatives. The recent finding that 5hmC is also a stable and independent epigenetic modification indicates that these proteins play an important role in diverse physiological and pathological processes such as neural and tumor development. Both the genomic distribution of (hydroxy)methylation and the expression and activity of TET proteins are dysregulated in a wide range of cancers including prostate cancer. Up to now it is still unknown how changes in TET and 5(h)mC profiles are related to the pathogenesis of prostate cancer. In this review, we explore recent advances in the current understanding of how TET expression and function are regulated in development and cancer. Furthermore, we look at the impact on 5hmC in prostate cancer and the potential underlying mechanisms. Finally, we tried to summarize the latest techniques for detecting and quantifying global and locus-specific 5hmC levels of genomic DNA.
Citation
Smeets , E , Lynch , A G , Prekovic , S , Van den Broeck , T , Moris , L , Helsen , C , Joniau , S , Claessens , F & Massie , C E 2018 , ' The role of TET-mediated DNA hydroxymethylation in prostate cancer ' , Molecular and Cellular Endocrinology , vol. 462 , no. A , pp. 41-55 . https://doi.org/10.1016/j.mce.2017.08.021
Publication
Molecular and Cellular Endocrinology
Status
Peer reviewed
DOI
https://doi.org/10.1016/j.mce.2017.08.021
ISSN
0303-7207
Type
Journal item
Rights
© 2017 Elsevier Ltd. This work has been made available online in accordance with the publisher’s policies. This is the author created, accepted version manuscript following peer review and may differ slightly from the final published version. The final published version of this work is available at https://doi.org/10.1016/j.mce.2017.08.021
Description
Massie C. is funded by an ERC grant (337905) and acknowledges support of the University of Cambridge, the Cancer Research UK Cambridge Centre and Hutchison Whampoa Limited. Claessens F. and Joniau S. hold grants from Fonds Wetenschappelijk Onderzoek-Vlaanderen (GOA9816N, G.0684.12N, G.0830.13N). Van den Broeck T. is supported by a PhD fellowship from Fonds Wetenschappelijk Onderzoek-Vlaanderen (11ZO616N). This work was also supported by the KU Leuven (GOA/15/017) and Kom op tegen Kanker.
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  • University of St Andrews Research
URI
http://hdl.handle.net/10023/15937

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