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H3K4 histone methylation in oral squamous cell carcinoma.
Author(s) -
Marta Mancuso,
Danilo Swann Matassa,
Mariachiara Conte,
G Colella,
Gina Rana,
Laura Fucci,
Marina Piscopo
Publication year - 2009
Publication title -
acta biochimica polonica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.452
H-Index - 78
eISSN - 1734-154X
pISSN - 0001-527X
DOI - 10.18388/abp.2009_2473
Subject(s) - h3k4me3 , histone , epigenetics , methylation , histone methylation , chromatin , basal cell , cancer , dna methylation , biology , cancer research , chemistry , medicine , genetics , dna , gene expression , gene , promoter
Methylation of specific lysine residues in histone tails has been proposed to function as a stable epigenetic marker that directs biological functions altering chromatin structure. Recent findings have implicated alteration in heterochromatin formation as a contributing factor in cancer development. In order to verify whether changes in the overall level of H3K4 histone methylation could be involved in oral squamous carcinoma, the levels of H3K4me1, me2 and me3 were measured in oral squamous carcinoma, leukoplakias and normal tissues. The levels of H3K4me2 and me3 were significantly different in oral squamous cell carcinoma in comparison with normal tissue: the level of H3K4me2 was increased while that of H3K4me3 decreased. No significant differences could be found between the two types of tissues in the level of H3K4me1. A similar trend was found in the leukoplakias that appeared more like the pathological than normal tissue. These results support the idea that alteration of chromatin structure could contribute to oncogenic potential.

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