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Transition to naïve human pluripotency mirrors pan-cancer DNA hypermethylation

Research output: Contribution to Journal/Magazine › Journal article › peer-review

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Transition to naïve human pluripotency mirrors pan-cancer DNA hypermethylation. / Patani, H.; Rushton, M.D.; Higham, J. et al.
In: Nature Communications, Vol. 11, 3671, 22.07.2020.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Patani, H, Rushton, MD, Higham, J, Teijeiro, SA, Oxley, D, Cutillas, P, Sproul, D & Ficz, G 2020, 'Transition to naïve human pluripotency mirrors pan-cancer DNA hypermethylation', Nature Communications, vol. 11, 3671. https://doi.org/10.1038/s41467-020-17269-3

APA

Patani, H., Rushton, M. D., Higham, J., Teijeiro, S. A., Oxley, D., Cutillas, P., Sproul, D., & Ficz, G. (2020). Transition to naïve human pluripotency mirrors pan-cancer DNA hypermethylation. Nature Communications, 11, Article 3671. https://doi.org/10.1038/s41467-020-17269-3

Vancouver

Patani H, Rushton MD, Higham J, Teijeiro SA, Oxley D, Cutillas P et al. Transition to naïve human pluripotency mirrors pan-cancer DNA hypermethylation. Nature Communications. 2020 Jul 22;11:3671. doi: 10.1038/s41467-020-17269-3

Author

Patani, H. ; Rushton, M.D. ; Higham, J. et al. / Transition to naïve human pluripotency mirrors pan-cancer DNA hypermethylation. In: Nature Communications. 2020 ; Vol. 11.

Bibtex

@article{24556f8b72004231b572508e749d8b0f,
title = "Transition to na{\"i}ve human pluripotency mirrors pan-cancer DNA hypermethylation",
abstract = "Epigenetic reprogramming is a cancer hallmark, but how it unfolds during early neoplastic events and its role in carcinogenesis and cancer progression is not fully understood. Here we show that resetting from primed to na{\"i}ve human pluripotency results in acquisition of a DNA methylation landscape mirroring the cancer DNA methylome, with gradual hypermethylation of bivalent developmental genes. We identify a dichotomy between bivalent genes that do and do not become hypermethylated, which is also mirrored in cancer. We find that loss of H3K4me3 at bivalent regions is associated with gain of methylation. Additionally, we observe that promoter CpG island hypermethylation is not restricted solely to emerging na{\"i}ve cells, suggesting that it is a feature of a heterogeneous intermediate population during resetting. These results indicate that transition to na{\"i}ve pluripotency and oncogenic transformation share common epigenetic trajectories, which implicates reprogramming and the pluripotency network as a central hub in cancer formation.",
author = "H. Patani and M.D. Rushton and J. Higham and S.A. Teijeiro and D. Oxley and P. Cutillas and D. Sproul and G. Ficz",
year = "2020",
month = jul,
day = "22",
doi = "10.1038/s41467-020-17269-3",
language = "English",
volume = "11",
journal = "Nature Communications",
issn = "2041-1723",
publisher = "Nature Publishing Group",

}

RIS

TY - JOUR

T1 - Transition to naïve human pluripotency mirrors pan-cancer DNA hypermethylation

AU - Patani, H.

AU - Rushton, M.D.

AU - Higham, J.

AU - Teijeiro, S.A.

AU - Oxley, D.

AU - Cutillas, P.

AU - Sproul, D.

AU - Ficz, G.

PY - 2020/7/22

Y1 - 2020/7/22

N2 - Epigenetic reprogramming is a cancer hallmark, but how it unfolds during early neoplastic events and its role in carcinogenesis and cancer progression is not fully understood. Here we show that resetting from primed to naïve human pluripotency results in acquisition of a DNA methylation landscape mirroring the cancer DNA methylome, with gradual hypermethylation of bivalent developmental genes. We identify a dichotomy between bivalent genes that do and do not become hypermethylated, which is also mirrored in cancer. We find that loss of H3K4me3 at bivalent regions is associated with gain of methylation. Additionally, we observe that promoter CpG island hypermethylation is not restricted solely to emerging naïve cells, suggesting that it is a feature of a heterogeneous intermediate population during resetting. These results indicate that transition to naïve pluripotency and oncogenic transformation share common epigenetic trajectories, which implicates reprogramming and the pluripotency network as a central hub in cancer formation.

AB - Epigenetic reprogramming is a cancer hallmark, but how it unfolds during early neoplastic events and its role in carcinogenesis and cancer progression is not fully understood. Here we show that resetting from primed to naïve human pluripotency results in acquisition of a DNA methylation landscape mirroring the cancer DNA methylome, with gradual hypermethylation of bivalent developmental genes. We identify a dichotomy between bivalent genes that do and do not become hypermethylated, which is also mirrored in cancer. We find that loss of H3K4me3 at bivalent regions is associated with gain of methylation. Additionally, we observe that promoter CpG island hypermethylation is not restricted solely to emerging naïve cells, suggesting that it is a feature of a heterogeneous intermediate population during resetting. These results indicate that transition to naïve pluripotency and oncogenic transformation share common epigenetic trajectories, which implicates reprogramming and the pluripotency network as a central hub in cancer formation.

U2 - 10.1038/s41467-020-17269-3

DO - 10.1038/s41467-020-17269-3

M3 - Journal article

VL - 11

JO - Nature Communications

JF - Nature Communications

SN - 2041-1723

M1 - 3671

ER -