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Review
. 2017 May 30;8(44):78163-78173.
doi: 10.18632/oncotarget.18293. eCollection 2017 Sep 29.

DNA methylation/hydroxymethylation in melanoma

Affiliations
Review

DNA methylation/hydroxymethylation in melanoma

Siqi Fu et al. Oncotarget. .

Abstract

Melanoma is a malignant tumor of melanocytes and is considered to be the most aggressive cancer among all skin diseases. The pathogenesis of melanoma has not been well documented, which may restrict the research and development of biomarkers and therapies. To date, several genetic and epigenetic factors have been identified as contributing to the development and progression of melanoma. Besides the findings on genetic susceptibilities, the recent progress in epigenetic studies has revealed that loss of the DNA hydroxymethylation mark, 5-hydroxymethylcytosine (5-hmC), along with high levels of DNA methylation at promoter regions of several tumor suppressor genes in melanoma, may serve as biomarkers for melanoma. Moreover, 5-Aza-2'-deoxycytidine, an epigenetic modifier causing DNA demethylation, and ten-eleven translocation family dioxygenase (TET), which catalyzes the generation of 5-hmC, demonstrate therapeutic potential in melanoma treatment. In this review, we will summarize the latest progress in research on DNA methylation/hydroxymethylation in melanoma, and we will discuss and provide insight for epigenetic biomarkers and therapies for melanoma. Particularly, we will discuss the role of DNA hydroxymethylation in melanoma infiltrating immune cells, which may also serve as a potential target for melanoma treatment.

Keywords: 5-hmC; 5-mC; TET; epigenetic therapy; melanoma.

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Conflict of interest statement

CONFLICTS OF INTEREST The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1. The CpG islands and CpG island shores
Figure 2
Figure 2. How DNA methylation regulates transcription
Figure 3
Figure 3. The cycle of DNA methylation and demethylation

References

    1. Raimondi S, Sera F, Gandini S, Iodice S, Caini S, Maisonneuve P, Fargnoli MC. MC1R variants, melanoma and red hair color phenotype: a meta-analysis. Int J Cancer. 2008;122:2753–60. - PubMed
    1. Pfeifer GP. How the environment shapes cancer genomes. Curr Opin Oncol. 2015;27:71–7. - PMC - PubMed
    1. Hernando B, Ibarrola-Villava M, Fernandez LP, Pena-Chilet M, Llorca-Cardenosa M, Oltra SS, Alonso S, Boyano MD, Martinez-Cadenas C, Ribas G. Sex-specific genetic effects associated with pigmentation, sensitivity to sunlight, and melanoma in a population of Spanish origin. Biol Sex Differ. 2016;7:17. - PMC - PubMed
    1. Pleasance ED, Cheetham RK, Stephens PJ, McBride DJ, Humphray SJ, Greenman CD, Varela I, Lin ML, Ordonez GR, Bignell GR, Ye K, Alipaz J, Bauer MJ, et al. A comprehensive catalogue of somatic mutations from a human cancer genome. Nature. 2010;463:191–6. - PMC - PubMed
    1. Hodis E, Watson IR, Kryukov GV, Arold ST, Imielinski M, Theurillat JP, Nickerson E, Auclair D, Li L, Place C, Dicara D, Ramos AH, Lawrence MS, et al. A landscape of driver mutations in melanoma. Cell. 2012;150:251–63. - PMC - PubMed

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