File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

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

TitleTriptolide alters histone H3K9 and H3K27 methylation state and induces G0/G1 arrest and caspase-dependent apoptosis in multiple myeloma in vitro
Authors
KeywordsEzh2
Histone Methylation
Multiple Myeloma
Suv39h1
Triptolide
Issue Date2009
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/toxicol
Citation
Toxicology, 2009 How to Cite?
AbstractTriptolide 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. © 2009 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/92068
ISSN
2015 Impact Factor: 3.817
2015 SCImago Journal Rankings: 1.335
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Sciences Foundation of China30700882
Funding Information:

This work was supported by a grant from the National Natural Sciences Foundation of China (no. 30700882). The authors would like to thank the Department of Central Laboratory, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China, for offering relevant experimental facilities and technical support.

 

DC FieldValueLanguage
dc.contributor.authorZhao, Fen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorLi, Ren_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorWen, Len_HK
dc.contributor.authorZhang, Cen_HK
dc.date.accessioned2010-09-17T10:35:08Z-
dc.date.available2010-09-17T10:35:08Z-
dc.date.issued2009en_HK
dc.identifier.citationToxicology, 2009en_HK
dc.identifier.issn0300-483Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/92068-
dc.description.abstractTriptolide 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. © 2009 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/toxicolen_HK
dc.relation.ispartofToxicologyen_HK
dc.subjectEzh2en_HK
dc.subjectHistone Methylationen_HK
dc.subjectMultiple Myelomaen_HK
dc.subjectSuv39h1en_HK
dc.subjectTriptolideen_HK
dc.titleTriptolide alters histone H3K9 and H3K27 methylation state and induces G0/G1 arrest and caspase-dependent apoptosis in multiple myeloma in vitroen_HK
dc.typeArticleen_HK
dc.identifier.emailChen, Y:ychenc@hkucc.hku.hken_HK
dc.identifier.authorityChen, Y=rp1318en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.tox.2009.10.023en_HK
dc.identifier.pmid19879315-
dc.identifier.scopuseid_2-s2.0-71849116889-
dc.identifier.isiWOS:000274588700010-
dc.identifier.citeulike6195448-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats