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Toxicology. 2010 Jan 12;267(1-3):70-9. doi: 10.1016/j.tox.2009.10.023. Epub 2009 Oct 29.

Triptolide alters histone H3K9 and H3K27 methylation state and induces G0/G1 arrest and caspase-dependent apoptosis in multiple myeloma in vitro.

Author information

1
Department of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Abstract

Triptolide is the principal active ingredient in extracts from the Chinese herb Tripterygium wilfordii Hook.F (TwHF), and has various functions such as immunosuppression, anti-inflammatory and antitumor properties. In diverse hematological tumors triptolide exerts antitumor activity and many studies have tried to elucidate the potential antitumor mechanism. The evidence that triptolide-induced gene promoter DNA hypermethylation has suggested that epigenetic mechanisms may play an important role in the antitumor activity of triptolide. Our study aimed to investigate the association of the therapeutic effect of triptolide on multiple myeloma with the regulation of histone methylation. Triptolide inhibited the proliferation of multiple myeloma cell line RPMI8226 in a time- and dose-dependent manner, induced G0/G1 cell cycle arrest and apoptosis. Triptolide decreased histone H3K9 and H3K27 methylation via the downregulation of histone methyltransferase SUV39H1 and EZH2, respectively, which possibly was the anti-myeloma mechanism of triptolide.

PMID:
19879315
DOI:
10.1016/j.tox.2009.10.023
[Indexed for MEDLINE]

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