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Article: Curcumin-induced histone acetylation in malignant hematologic cells

TitleCurcumin-induced histone acetylation in malignant hematologic cells
Authors
KeywordsCurcumin
Histone Acetylation
Histone Deacetylation
Issue Date2009
Citation
Journal of Huazhong University of Science and Technology - Medical Science, 2009, v. 29 n. 1, p. 25-28 How to Cite?
AbstractThis study investigated the inhibitory effects of curcumin on proliferation of hematological malignant cells in vitro and the anti-tumor mechanism at histone acetylation/histone deacetylation levels. The effects of curcumin and histone deacetylase inhibitor trichostatin A (TSA) on the growth of Raji cells were tested by MTT assay. The expression of acetylated histone-3 (H3) in Raji, HL60 and K562 cells, and peripheral blood mononuclear cells (PBMCs) treated with curcumin or TSA was detected by immunohistochemistry and FACS. The results showed curcumin inhibited proliferation of Raji cells significantly in a time- and dose-dependent fashion, while exhibited low toxicity in PBMCs. Curcumin induced up-regulation of the expression of acetylated H3 dose-dependently in all malignant cell lines tested. In conclusion, curcumin inhibited proliferation of Raji cells selectively, enhanced the level of acetylated (H3) in Raji, HL60, and K562 cells, which acted as a histone deacetylase inhibitor like TSA. Furthermore, up-regulation of H 3 acetylation may play an important role in regulating the proliferation of Raji cells. © 2009 Huazhong University of Science and Technology and Springer-Verlag GmbH.
Persistent Identifierhttp://hdl.handle.net/10722/92346
ISSN
2019 Impact Factor: 1.151
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHu, Jen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorChen, Yen_HK
dc.date.accessioned2010-09-17T10:43:20Z-
dc.date.available2010-09-17T10:43:20Z-
dc.date.issued2009en_HK
dc.identifier.citationJournal of Huazhong University of Science and Technology - Medical Science, 2009, v. 29 n. 1, p. 25-28en_HK
dc.identifier.issn1672-0733en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92346-
dc.description.abstractThis study investigated the inhibitory effects of curcumin on proliferation of hematological malignant cells in vitro and the anti-tumor mechanism at histone acetylation/histone deacetylation levels. The effects of curcumin and histone deacetylase inhibitor trichostatin A (TSA) on the growth of Raji cells were tested by MTT assay. The expression of acetylated histone-3 (H3) in Raji, HL60 and K562 cells, and peripheral blood mononuclear cells (PBMCs) treated with curcumin or TSA was detected by immunohistochemistry and FACS. The results showed curcumin inhibited proliferation of Raji cells significantly in a time- and dose-dependent fashion, while exhibited low toxicity in PBMCs. Curcumin induced up-regulation of the expression of acetylated H3 dose-dependently in all malignant cell lines tested. In conclusion, curcumin inhibited proliferation of Raji cells selectively, enhanced the level of acetylated (H3) in Raji, HL60, and K562 cells, which acted as a histone deacetylase inhibitor like TSA. Furthermore, up-regulation of H 3 acetylation may play an important role in regulating the proliferation of Raji cells. © 2009 Huazhong University of Science and Technology and Springer-Verlag GmbH.en_HK
dc.languageengen_HK
dc.relation.ispartofJournal of Huazhong University of Science and Technology - Medical Scienceen_HK
dc.subjectCurcuminen_HK
dc.subjectHistone Acetylationen_HK
dc.subjectHistone Deacetylationen_HK
dc.titleCurcumin-induced histone acetylation in malignant hematologic cellsen_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.doi10.1007/s11596-009-0105-5en_HK
dc.identifier.pmid19224157-
dc.identifier.scopuseid_2-s2.0-67650620708en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67650620708&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume29en_HK
dc.identifier.issue1en_HK
dc.identifier.spage25en_HK
dc.identifier.epage28en_HK
dc.identifier.isiWOS:000263509100005-
dc.identifier.citeulike4088693-
dc.identifier.issnl1672-0733-

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