Journal
BIOSCIENCE REPORTS
Volume 35, Issue -, Pages -Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BSR20150064
Keywords
diazepin-quinazolin-amine derivative (BIX-01294); cellular toxicity; DNA methylation; histone dimethylation; mouse embryonic fibroblasts; Snrpn
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Funding
- National Natural Science Foundation of China [31071311]
- Natural Science Foundation of Fujian Province of China [2009J06017]
- Science and Technology Plan of Fuzhou [2014-S-146]
- Key Clinical Speciality Discipline Construction Program of Fujian [2014J01313]
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Histone H3 lysine 9 dimethylation (H3K9me2) hypermethylation is thought to be a major influential factor in cellular reprogramming, such as somatic cell nuclear transfer (SCNT) and induction of pluripotent stem cells (iPSCs). The diazepin-quinazolin-amine derivative (BIX-01294) specifically inhibits the activity of histone methyltransferase EHMT2 (euchromatic histone-lysine N-methyltransferase 2) and reduces H3K9me2 levels in cells. The imprinted gene small nuclear ribonucleoprotein N (Snrpn) is of particular interest because of its important biological functions. The objective of the present study was to investigate the effect of BIX-01294 on H3K9me2 levels and changes in Snrpn DNA methylation and histone H3K9me2 in mouse embryonic fibroblasts (MEFs). Results showed that 1.3 mu M BIX-01294 markedly reduced global levels of H3K9me2 with almost no cellular toxicity. There was a significant decrease in H3K9me2 in promoter regions of the Snrpn gene after BIX-01294 treatment. A significant increase in methylation of the Snrpn differentially methylated region 1 (DMR1) and slightly decreased transcript levels of Snrpn were found in BIX-01294-treated MEFs. These results suggest that BIX-01294 may reduce global levels of H3K9me2 and affect epigenetic modifications of Snrpn in MEFs.
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