The role of TET-mediated DNA hydroxymethylation in prostate cancer

E. Smeets; A. G. Lynch; S. Prekovic; T. Van den Broeck; L Moris; C. Helsen; S. Joniau; F. Claessens; C. E. Massie

doi:10.1016/j.mce.2017.08.021

The role of TET-mediated DNA hydroxymethylation in prostate cancer

E. Smeets, A. G. Lynch, S. Prekovic, T. Van den Broeck, L Moris, C. Helsen, S. Joniau, F. Claessens, C. E. Massie

Research output: Contribution to journal › Review article › peer-review

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.

Original language	English
Pages (from-to)	41-55
Journal	Molecular and Cellular Endocrinology
Volume	462
Issue number	A
Early online date	1 Sept 2017
DOIs	https://doi.org/10.1016/j.mce.2017.08.021
Publication status	Published - 15 Feb 2018

Keywords

Prostate cancer
Epigenetics
TET
DNA hydroxymethylation
5hmC

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.mce.2017.08.021

Lynch_2017_MCE_TET-mediated_AAM
© 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
Accepted author manuscript, 2.01 MBLicence: CC BY-NC-ND

Cite this

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title = "The role of TET-mediated DNA hydroxymethylation in prostate cancer",

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.",

keywords = "Prostate cancer, Epigenetics, TET, DNA hydroxymethylation, 5hmC",

author = "E. Smeets and Lynch, {A. G.} and S. Prekovic and {Van den Broeck}, T. and L Moris and C. Helsen and S. Joniau and F. Claessens and Massie, {C. E.}",

note = "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.",

year = "2018",

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doi = "10.1016/j.mce.2017.08.021",

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T1 - The role of TET-mediated DNA hydroxymethylation in prostate cancer

AU - Smeets, E.

AU - Lynch, A. G.

AU - Prekovic, S.

AU - Van den Broeck, T.

AU - Moris, L

AU - Helsen, C.

AU - Joniau, S.

AU - Claessens, F.

AU - Massie, C. E.

N1 - 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.

PY - 2018/2/15

Y1 - 2018/2/15

N2 - 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.

AB - 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.

KW - Prostate cancer

KW - Epigenetics

KW - TET

KW - DNA hydroxymethylation

KW - 5hmC

U2 - 10.1016/j.mce.2017.08.021

DO - 10.1016/j.mce.2017.08.021

M3 - Review article

C2 - 28870782

SN - 0303-7207

VL - 462

SP - 41

EP - 55

JO - Molecular and Cellular Endocrinology

JF - Molecular and Cellular Endocrinology

IS - A

ER -

The role of TET-mediated DNA hydroxymethylation in prostate cancer

Abstract

Keywords

UN SDGs

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