Nucleosome positioning changes during human embryonic stem cell differentiation

Zhang, Wenjuan; Li, Yaping; Kulik, Michael; Tiedemann, Rochelle L.; Robertson, Keith D.; Dalton, Stephen; Zhao, Shaying

doi:10.1080/15592294.2016.1176649

Cited by 7 publications

(3 citation statements)

References 69 publications

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“…For nucleosome analysis, we collected a panel of 29 MNase-seq profiles of various human tissues and cell types (including two sperm samples) (ENCODE Consortium, 2012;Descostes et al, 2014;Diermeier et al, 2014;Du et al, 2017;Gaffney et al, 2012;Gaidatzis et al, 2014;Gomez et al, 2016;Hammoud et al, 2009;Hu et al, 2011;Jiang et al, 2018;Jung et al, 2012;Kelly et al, 2012;Kfir et al, 2015;Lavender et al, 2016;Shah et al, 2018;West et al, 2014;Yazdi et al, 2015;Zhang et al, 2016). The raw reads for all these samples were downloaded from the SRA database (the SRR run IDs are provided in Table S5).…”

Section: Super-enhancer Erna Expression Profilesmentioning

confidence: 99%

A High-Resolution Map of Human Enhancer RNA Loci Characterizes Super-enhancer Activities in Cancer

Chen

Liang

2020

Cancer Cell

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Section: Super-enhancer Erna Expression Profilesmentioning

confidence: 99%

A High-Resolution Map of Human Enhancer RNA Loci Characterizes Super-enhancer Activities in Cancer

Chen

Liang

2020

Cancer Cell

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“…This complex contains ARID1A protein, which can inhibit SOX2 and OCT4 gene expression to promote differentiation [ 102 ]. This feature is also required for cellular differentiation during embryonic development [ 103 , 104 ].…”

Section: Epigenetic Similarities Between Early Human Development and Cancermentioning

confidence: 99%

Can Immune Suppression and Epigenome Regulation in Placenta Offer Novel Insights into Cancer Immune Evasion and Immunotherapy Resistance?

et al. 2021

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Cancer is the second leading cause of mortality and morbidity in the developed world. Cancer progression involves genetic and epigenetic alterations, accompanied by aggressive changes, such as increased immune evasion, onset of metastasis, and drug resistance. Similar to cancer, DNA hypomethylation, immune suppression, and invasive cell behaviours are also observed in the human placenta. Mechanisms that lead to the acquisition of invasive behaviour, immune evasion, and drug and immunotherapy resistance are presently under intense investigations to improve patient outcomes. Here, we review current knowledge regarding the similarities between immune suppression and epigenome regulation, including the expression of repetitive elements (REs), endogenous retroviruses (ERVs) and transposable elements (TEs) in cells of the placenta and in cancer, which are associated with changes in immune regulation and invasiveness. We explore whether immune suppression and epigenome regulation in placenta offers novel insights into immunotherapy resistance in cancer, and we also discuss the implications and the knowledge gaps relevant to these findings, which are rapidly being accrued in these quite disparate research fields. Finally, we discuss potential linkages between TE, ERV and RE activation and expression, regarding mechanisms of immune regulation in placenta and cancer. A greater understanding of the role of immune suppression and associated epigenome regulation in placenta could help to elucidate some comparable mechanisms operating in cancer, and identify potential new therapeutic targets for treating cancer.

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“…While small-scale chromatin changes at DNA regulatory elements occur during transcriptional regulation in most cells, extensive remodelling of chromatin structure is required for cellular differentiation during embryonic development. [72][73][74] In particular, the SWI/SNF remodelling complex is known to be important in ESCs and development: SWI/SNF complexes containing the ARID1A protein can remodel chromatin to inhibit expression of the pluripotency genes Sox2 and Oct4, and promote differentiation to mesoderm, but not ectoderm. 75 Nucleosome positioning is also important in the reprogramming of somatic cells to pluripotency.…”

Section: Nucleosome Positioning and Histone Variants In Csc Plasticitymentioning

confidence: 99%

Epigenetic regulation of cancer stem cell formation and maintenance

French

Pauklin

2020

Intl Journal of Cancer

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Cancerous tumours contain a rare subset of cells with stem-like properties that are termed cancer stem cells (CSCs). CSCs are defined by their ability to divide both symmetrically and asymmetrically, to initiate new tumour growth and to tolerate the foreign niches required for metastatic dissemination. Accumulating evidence suggests that tumours arise from cells with stem-like properties, the generation of CSCs is therefore likely to be an initiatory event in carcinogenesis. Furthermore, CSCs in established tumours exist in a dynamic and plastic state, with nonstem tumour cells thought to be capable of de-differentiation to CSCs. The regulation of the CSC state both during tumour initiation and within established tumours is a desirable therapeutic target and is mediated by epigenetic factors. In this review, we will explore the epigenetic parallels between induced pluripotency and the generation of CSCs, and discuss how the epigenetic regulation of CSCs opens up novel opportunities for therapeutic intervention. K E Y W O R D S cancer stem cells, cancer therapy, early detection of cancer, epigenetics, induced pluripotent stem cells, tumorigenesis 1 | INTRODUCTION As with adult tissues, cancerous tumours also contain a rare subset of cells with stem-like properties that can function to regenerate the heterogeneous cell populations observed therein. These cancer stem cells (CSCs) are defined by their ability to divide both symmetrically and asymmetrically, to initiate new tumour growth and to tolerate the foreign niches required for metastatic dissemination. As the tumourinitiating population, CSCs underpin the very nature of malignancy and studying their regulation is essential for understanding tumour formation, metastasis and relapse after therapy. As it is not possible to isolate CSCs based on functional properties, CSC identification can be achieved by FACs sorting based on surrogate cell surface marker profiles and subsequent transplantation into immune-compromised mice to demonstrate enhanced tumourigenic potential. Using this strategy, CSCs have been identified in most cancers, first in acute myeloid leukaemia (AML) followed by breast cancer and other solid malignancies such as brain, colon and pancreatic cancer, and are purported to account for only a few per cent of the total cell population.

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Nucleosome positioning changes during human embryonic stem cell differentiation

Cited by 7 publications

References 69 publications

A High-Resolution Map of Human Enhancer RNA Loci Characterizes Super-enhancer Activities in Cancer

A High-Resolution Map of Human Enhancer RNA Loci Characterizes Super-enhancer Activities in Cancer

Can Immune Suppression and Epigenome Regulation in Placenta Offer Novel Insights into Cancer Immune Evasion and Immunotherapy Resistance?

Epigenetic regulation of cancer stem cell formation and maintenance

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