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Review
. 2017 Feb 1;16(1):29.
doi: 10.1186/s12943-017-0596-9.

Epigenetics in cancer stem cells

Tan Boon Toh  1 , Jhin Jieh Lim  1 , Edward Kai-Hua Chow  2   3   4
Affiliations
Review

Epigenetics in cancer stem cells

Tan Boon Toh et al. Mol Cancer. .

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.

Keywords: Cancer stem cells; DNA methylation; Epigenetics; Histone methylation; Histone methyltransferase; Signaling pathway.

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Figures

Fig. 1
Fig. 1
Regulation of key cancer stem cell signaling pathways by epigenetic mechanisms. Wnt/β-catenin signaling can be enhanced by decreased expression of the DKK1 inhibitor through promoter hypermethylation and increased H3K27me3 and decreased H3K16 acetylation marks. Notch signaling target genes such as Hes1 and Hes5 can be activated by inhibition of H3K27 inhibitory methylation mark at their promoter region by STRAP. Hedgehog signaling pathway can be activated in CSCs epigenetically by Shh promoter hypomethylation and increase HDAC1 expression. Epigenetic deregulation of CSC-related signaling pathways allows cancer cells to acquire self-renewal ability and drug resistance properties
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