Histone Post-Translational Modifications and Cancer

Lucia Armelin-Correa^1* & Cleiton Fagundes Machado^2*

¹Cellular Biology Department - UNIFESP Diadema, Brazil
²Department of Biochemistry of the University of Sao Paulo - USP, Brazil

Dr. Lucia Armelin-Correa, Cellular Biology Department - UNIFESP Diadema, Brazil & Dr. Cleiton Fagundes Machado, Department of Biochemistry of the University of Sao Paulo - USP, Brazil.

Keywords: Cancer; Epigenetics; Heterochromatin; Enhancer of Zeste Homolog 2; Histone-Modifying Ezymes; Suppressor of Variegation 3/9; Epidrugs

Abstract

Epigenetic involves mechanisms which control gene transcription but convey no changes in the DNA sequences. A series of epigenetic modifications have been described in several tumors and this knowledge is important for the adequate diagnosis and treatment of the disease. The epigenetic mechanisms involve, among others processes, histone modifications, such as the trimethylation of histone 3 lysine 9 (H3K9me3) and lysine 27 (H3K27me3), characteristics of constitutive and facultative heterochromatin, respectively, which are associated with gene silencing. Suppressor of Variegation 3-9 homolog 1 and 2 (SUV39H1, SUV39H2) are critical enzymes for trimethylation of H3K9, while Polycomb Repressor Complex 2 (PRC2) is responsible for the methylation of histone 3 lysine 27. These histone-modifying enzymes are evolutionarily conserved and their misexpression, as well as that of their corresponding histone marks, have been associated with different types of cancer, which leads us to believe that histone-modifying enzymes are promising targets for oncologic drugs.

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