Epigenetics in cancer stem cells

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Abstract

Compelling evidence have demonstrated that bulk tumors can arise from a unique subset of cells commonly termed “cancer stem cells” that has been proposed to be a strong driving force of tumorigenesis and a key mechanism of therapeutic resistance. Recent advances in epigenomics have illuminated key mechanisms by which epigenetic regulation contribute to cancer progression. In this review, we present a discussion of how deregulation of various epigenetic pathways can contribute to cancer initiation and tumorigenesis, particularly with respect to maintenance and survival of cancer stem cells. This information, together with several promising clinical and preclinical trials of epigenetic modulating drugs, offer new possibilities for targeting cancer stem cells as well as improving cancer therapy overall.

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Most cited references 189

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Epithelial-mesenchymal transitions in development and disease.

Jean Paul Thiery, Hervé Acloque, Ruby Y J Huang … (2009)

The epithelial to mesenchymal transition (EMT) plays crucial roles in the formation of the body plan and in the differentiation of multiple tissues and organs. EMT also contributes to tissue repair, but it can adversely cause organ fibrosis and promote carcinoma progression through a variety of mechanisms. EMT endows cells with migratory and invasive properties, induces stem cell properties, prevents apoptosis and senescence, and contributes to immunosuppression. Thus, the mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.

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Epigenetics in cancer.

S. Sharma, T. Kelly, P. Jones (2010)

Epigenetic mechanisms are essential for normal development and maintenance of tissue-specific gene expression patterns in mammals. Disruption of epigenetic processes can lead to altered gene function and malignant cellular transformation. Global changes in the epigenetic landscape are a hallmark of cancer. The initiation and progression of cancer, traditionally seen as a genetic disease, is now realized to involve epigenetic abnormalities along with genetic alterations. Recent advancements in the rapidly evolving field of cancer epigenetics have shown extensive reprogramming of every component of the epigenetic machinery in cancer including DNA methylation, histone modifications, nucleosome positioning and non-coding RNAs, specifically microRNA expression. The reversible nature of epigenetic aberrations has led to the emergence of the promising field of epigenetic therapy, which is already making progress with the recent FDA approval of three epigenetic drugs for cancer treatment. In this review, we discuss the current understanding of alterations in the epigenetic landscape that occur in cancer compared with normal cells, the roles of these changes in cancer initiation and progression, including the cancer stem cell model, and the potential use of this knowledge in designing more effective treatment strategies.

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Stability and flexibility of epigenetic gene regulation in mammalian development.

Wolf Reik (2007)

During development, cells start in a pluripotent state, from which they can differentiate into many cell types, and progressively develop a narrower potential. Their gene-expression programmes become more defined, restricted and, potentially, 'locked in'. Pluripotent stem cells express genes that encode a set of core transcription factors, while genes that are required later in development are repressed by histone marks, which confer short-term, and therefore flexible, epigenetic silencing. By contrast, the methylation of DNA confers long-term epigenetic silencing of particular sequences--transposons, imprinted genes and pluripotency-associated genes--in somatic cells. Long-term silencing can be reprogrammed by demethylation of DNA, and this process might involve DNA repair. It is not known whether any of the epigenetic marks has a primary role in determining cell and lineage commitment during development.

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Author and article information

Contributors

Tan Boon Toh: csittb@nus.edu.sg

Jhin Jieh Lim: csiljj@nus.edu.sg

Edward Kai-Hua Chow: +65 6516-8707 , csikce@nus.edu.sg

Journal

Journal ID (nlm-ta): Mol Cancer

Journal ID (iso-abbrev): Mol. Cancer

Title: Molecular Cancer

Publisher: BioMed Central (London )

ISSN (Electronic): 1476-4598

Publication date (Electronic): 1 February 2017

Publication date PMC-release: 1 February 2017

Publication date Collection: 2017

Volume: 16

Electronic Location Identifier: 29

Affiliations

[1 ]ISNI 0000 0001 2180 6431, GRID grid.4280.e, Cancer Science Institute of Singapore, , National University of Singapore, ; Singapore, Singapore

[2 ]ISNI 0000 0001 2180 6431, GRID grid.4280.e, Department of Pharmacology, Yong Loo Lin School of Medicine, , National University of Singapore, ; Singapore, Singapore

[3 ]ISNI 0000 0001 2180 6431, GRID grid.4280.e, Centre for Translational Medicine, , National University of Singapore, ; 14 Medical Drive #12-01, Singapore, 117599 Singapore

Article

Publisher ID: 596

DOI: 10.1186/s12943-017-0596-9

PMC ID: 5286794

PubMed ID: 28148257

SO-VID: be43d924-dca2-43ba-b558-0af0b152984f

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 5 October 2016

Date accepted : 19 January 2017

Funding

Funded by: Ministry of Education -Singapore (SG)

Award ID: MOE2015-T2-2-126

Funded by: Ministry of Education - Singapore (SG)

Award ID: T1-BSRG 2014-05

Custom metadata

ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: cancer stem cells,epigenetics,histone methylation,histone methyltransferase,dna methylation,signaling pathway

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ScienceOpen disciplines: Oncology & Radiotherapy

Keywords: cancer stem cells, epigenetics, histone methylation, histone methyltransferase, dna methylation, signaling pathway

Epigenetics in cancer stem cells

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Abstract

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Karger: Oncology

Most cited references 189

Epithelial-mesenchymal transitions in development and disease.

Epigenetics in cancer.

Stability and flexibility of epigenetic gene regulation in mammalian development.

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