Bivalent Epigenetic Control of Oncofetal Gene Expression in Cancer | Zendy

Sayyed K. Zaidi | Zendy; Seth Frietze | Zendy; Jonathan A. R. Gordon | Zendy; Jessica L. Heath | Zendy; Terri Messier | Zendy; Deli Hong | Zendy; Joseph R. Boyd | Zendy; Mingu Kang | Zendy; Anthony N. Imbalzano | Zendy; Jane B. Lian | Zendy; Janet L. Stein | Zendy; Gary S. Stein | Zendy

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Bivalent Epigenetic Control of Oncofetal Gene Expression in Cancer

Author(s) -

Sayyed K. Zaidi,

Seth Frietze,

Jonathan A. R. Gordon,

Jessica L. Heath,

Terri Messier,

Deli Hong,

Joseph R. Boyd,

Mingu Kang,

Anthony N. Imbalzano,

Jane B. Lian,

Janet L. Stein,

Gary S. Stein

Publication year - 2017

Publication title -

molecular and cellular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.14

H-Index - 327

eISSN - 1067-8824

pISSN - 0270-7306

DOI - 10.1128/mcb.00352-17

Subject(s) - bivalent chromatin , biology , epigenetics , chromatin , epigenetic regulation of neurogenesis , histone , bivalent (engine) , cancer epigenetics , epigenomics , induced pluripotent stem cell , h3k4me3 , cellular differentiation , genomic imprinting , dna methylation , regulation of gene expression , chromatin remodeling , genetics , microbiology and biotechnology , gene expression , gene , embryonic stem cell , histone methyltransferase , promoter , chemistry , organic chemistry , metal

Multiple mechanisms of epigenetic control that include DNA methylation, histone modification, noncoding RNAs, and mitotic gene bookmarking play pivotal roles in stringent gene regulation during lineage commitment and maintenance. Experimental evidence indicates that bivalent chromatin domains, i.e., genome regions that are marked by both H3K4me3 (activating) and H3K27me3 (repressive) histone modifications, are a key property of pluripotent stem cells. Bivalency of developmental genes during the G 1 phase of the pluripotent stem cell cycle contributes to cell fate decisions. Recently, some cancer types have been shown to exhibit partial recapitulation of bivalent chromatin modifications that are lost along with pluripotency, suggesting a mechanism by which cancer cells reacquire properties that are characteristic of undifferentiated, multipotent cells. This bivalent epigenetic control of oncofetal gene expression in cancer cells may offer novel insights into the onset and progression of cancer and may provide specific and selective options for diagnosis as well as for therapeutic intervention.

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