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Correlation between histone acetylation and expression of the MYO18B gene in human lung cancer cells
Author(s) -
Tani Masachika,
Ito Jun,
Nishioka Michiho,
Kohno Takashi,
Tachibana Ken,
Shiraishi Masahiko,
Takenoshita Seiichi,
Yokota Jun
Publication year - 2004
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/gcc.20027
Subject(s) - trichostatin a , acetylation , histone h4 , histone , biology , microbiology and biotechnology , cancer epigenetics , chromatin immunoprecipitation , epigenetics , histone h3 , sap30 , cancer research , gene silencing , carcinogenesis , histone deacetylase , hdac4 , histone h2a , gene expression , histone methyltransferase , promoter , gene , genetics
Recently, we isolated a candidate tumor‐suppressor gene, MYO18B , which was inactivated in approximately 50% of human lung cancers by deletion, mutation, and promoter methylation. However, more frequent reduction or loss of MYO18B expression and restoration of MYO18B expression by trichostatin A (TSA) treatment suggested the contribution of other mechanisms, especially histone deacetylation, for epigenetic inactivation of the MYO18B gene. In this study, we examined histone modification of the promoter region of the MYO18B gene in 8 human lung cancer cell lines by a chromatin immunoprecipitation assay. In 6 of 7 cell lines with reduced or silenced MYO18B expression, the levels of histones H3 and H4 acetylation surrounding the MYO18B promoter region were lower than those in a cell line with MYO18B expression. By treatment with TSA, the levels of histone H3 and H4 acetylation were increased in all 6 cell lines whose MYO18B expression was restored by TSA, whereas neither H3 nor H4 acetylation was increased in cells whose MYO18B expression was not restored by TSA. Significant correlations were observed between the levels of histone H3/H4 acetylation and MYO18B expression. These results suggest that acetylation of both histones H3 and H4 contributes to regulation of MYO18B expression in lung cancer cells and that histone deacetylation surrounding the promoter region plays an important role in MYO18B silencing and is involved in lung carcinogenesis. © 2004 Wiley‐Liss, Inc.