Chromatin remodeling through histone modification is an important mechanism of epigenetic gene dysregulation in @entity1 @entity5 . However, little is known about global alteration of histone status during tumorigenesis and @entity5 progression. Histone H3 status was examined in benign and malignant @entity14 by immunohistochemistry and Western blotting. For immunohistochemical evaluation, 4 anti-histone H3 antibodies, specific to dimethylation at @entity376 4 (H3K4me2), acetylation at @entity376 9 (H3K9ac), dimethylation at @entity376 9 (H3K9me2), and trimethylation at @entity376 27 (H3K27me3), were used. On immunohistochemistry, H3K4me2, H3K9ac, and H3K27me3 showed no significant changes between normal and @entity14 . On the other hand, the global level of H3K9me2 was distinctly higher in neoplastic cells ( @entity652 and @entity420 ) than in normal glandular cells. In addition, it was significantly higher in @entity420 than in @entity652 . Correspondingly, Western blotting confirmed that H3K9me2 expression was significantly higher in @entity420 than in normal colorectal mucosa. No alteration of H3K9me2 was observed with @entity5 differentiation and with the histological subtypes of @entity14 . These results suggest that aberration of the global H3K9me2 level is an important epigenetic event in colorectal tumorigenesis and @entity105 involved with gene regulation in neoplastic cells through chromatin remodeling.

Global histone modification of histone H3 in XXXX and its precursor lesions.

@entity1 :: ('9606', 'Species') :: ['human'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor', 'cancers', 'cancer'] @entity376 :: ('CHEBI:25094', 'Chemical') :: ['lysine'] @entity14 :: ('MESH:D015179', 'Disease') :: ['colorectal cancers', 'colorectal tumors'] @entity652 :: ('MESH:D000236', 'Disease') :: ['adenoma'] @entity105 :: ('MESH:D063646', 'Disease') :: ['carcinogenesis'] @entity420 :: ('MESH:D000230', 'Disease') :: ['adenocarcinomas', 'adenocarcinoma']
@entity14 :: (MESH:D015179,Disease) :: ['colorectal cancer']
