Proteomics

Dataset Information

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Proteomics of the transition to naïve human pluripotency


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 naïve human pluripotency results in acquisition of a DNA methylation landscape mirroring the cancer DNA methylome, with gradual hypermethylation of bivalent developmental genes. We hypothesised that unknown proteins and transcription factors play a role in the DNA hypermethylation process and analysed therefore the proteomics of the very early stages of the resetting process which involves overexpression of Nanog and Klf2. The samples analysed were Primed hESCs (Conventional stem cells), 72hours after induction and 1 week after induction, in triplicate. For our purposes we identified candidate transcription factors and subsequently knocked them down to test their involvement in the DNA hypermethylation (as described in the manuscript related to this data, Patani et al. Nature Communications). More broadly, we believe, this dataset is a useful resource for the wider community interested in pluripotency, resetting, reprogramming, cell identity transitions etc. Our 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.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo sapiens  

TISSUE(S): Embryonic Stem Cell

DISEASE(S): Not Available

SUBMITTER: Vinothini Rajeeve  

LAB HEAD: Dr Pedro R Cutillas

PROVIDER: PXD019893 | Pride | 2020-07-13

REPOSITORIES: pride

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Publications

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

Patani Hemalvi H   Rushton Michael D MD   Higham Jonathan J   Teijeiro Saul A SA   Oxley David D   Cutillas Pedro P   Sproul Duncan D   Ficz Gabriella G  

Nature communications 20200722 1


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  ...[more]

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