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Review
. 2018 Feb 3;19(2):459.
doi: 10.3390/ijms19020459.

Epigenetics and MicroRNAs in Cancer

Alice Ramassone  1   2 , Sara Pagotto  3   4 , Angelo Veronese  5   6 , Rosa Visone  7   8
Affiliations
Review

Epigenetics and MicroRNAs in Cancer

Alice Ramassone et al. Int J Mol Sci. .

Abstract

The ability to reprogram the transcriptional circuitry by remodeling the three-dimensional structure of the genome is exploited by cancer cells to promote tumorigenesis. This reprogramming occurs because of hereditable chromatin chemical modifications and the consequent formation of RNA-protein-DNA complexes that represent the principal actors of the epigenetic phenomena. In this regard, the deregulation of a transcribed non-coding RNA may be both cause and consequence of a cancer-related epigenetic alteration. This review summarizes recent findings that implicate microRNAs in the aberrant epigenetic regulation of cancer cells.

Keywords: epigenetics; human cancer; microRNAs.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Feedback circuit between microRNAs and epigenetic machinery. The epigenetic modification, such as promoter CpG island hyper- or hypo-methylation and/or histone modifications, affect miRNAs and genes transcription. MiRNAs can themselves regulate the epigenetic machinery by post-transcriptional gene silencing (PTGS), targeting DNMTs, HDACs, and the histone methyl-transferases (HMTs), establishing epigenetic pathway loops. In the figure, black lines represent the pathway starting from the epigenetic modifications and ending with the miRNAs maturation, while blue lines represent the pathway from the mature miRNA to the post transcriptional gene silencing of the epigenetic machinery.
Figure 2
Figure 2
MicroRNAs regulate gene transcription. Nuclear miRNAs can mediate both transcriptional gene silencing (TGS) and transcriptional gene activation (TGA) by targeting gene promoters. During the TGS, AGO1, DICER, EZH2, SUZ12, and YY1 proteins can be recruited on target promoters to induce the silencing through enrichment of H3K9me3 and H3K27me3. Instead, during the TGA, target promoters exhibit the enrichment of the RNA polymerase II, H3K4me3, and H3ac, H4ac; moreover, AGO1 was also found to be associated to target promoters during TGA. In the figure, black arrows indicate the miRNAs biogenesis pathway, and red and blue lines represent miRNAs translocated back to the nucleus to mediate TGS or TGA, respectively. Chromatin modifications are represented in bold.
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