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Article: Gambogic acid induces G0/G1 arrest and apoptosis involving inhibition of SRC-3 and inactivation of Akt pathway in K562 leukemia cells

TitleGambogic acid induces G0/G1 arrest and apoptosis involving inhibition of SRC-3 and inactivation of Akt pathway in K562 leukemia cells
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2009
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/toxicol
Citation
Toxicology, 2009, v. 262 n. 2, p. 98-105 How to Cite?
AbstractGambogic acid (GA), a major active component of gamboge, exhibits potent anticancer activity in many kinds of cancer cells. However, the anticancer mechanism of GA is not clearly understood. Here we showed that GA could cause growth inhibition, induce the G0/G1 phase cell cycle arrest and apoptosis in human chronic myelogenous leukemia cell line K562 cells. Since steroid receptor coactivator-3 (SRC-3), overexpressed in many human malignancies including leukemia, is a central target for cancer therapy, we also explored the effects of GA on SRC-3 and SRC-3-regulated gene products in K562. GA treatment downregulated the expression of SRC-3 and then inhibited the activity of Akt kinase and its downstream targets p70 S6 kinase 1 (S6K1) and glycogen synthase kinase 3β (GSK3β) without changes in total protein levels of these three proteins, which thus influenced the expression of the apoptosis related gene Bcl-2 in K562 cells. These results suggest that GA might exhibit its strong antitumor effects via the interruption of SRC-3. © 2009 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/92369
ISSN
2015 Impact Factor: 3.817
2015 SCImago Journal Rankings: 1.335
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Sciences Foundation of China30472267
Funding Information:

This work was supported by a grant from the National Natural Sciences Foundation of China (No. 30472267). 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.

References

 

DC FieldValueLanguage
dc.contributor.authorLi, Ren_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorZeng, L-len_HK
dc.contributor.authorShu, W-xen_HK
dc.contributor.authorZhao, Fen_HK
dc.contributor.authorWen, Len_HK
dc.contributor.authorLiu, Yen_HK
dc.date.accessioned2010-09-17T10:44:01Z-
dc.date.available2010-09-17T10:44:01Z-
dc.date.issued2009en_HK
dc.identifier.citationToxicology, 2009, v. 262 n. 2, p. 98-105en_HK
dc.identifier.issn0300-483Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/92369-
dc.description.abstractGambogic acid (GA), a major active component of gamboge, exhibits potent anticancer activity in many kinds of cancer cells. However, the anticancer mechanism of GA is not clearly understood. Here we showed that GA could cause growth inhibition, induce the G0/G1 phase cell cycle arrest and apoptosis in human chronic myelogenous leukemia cell line K562 cells. Since steroid receptor coactivator-3 (SRC-3), overexpressed in many human malignancies including leukemia, is a central target for cancer therapy, we also explored the effects of GA on SRC-3 and SRC-3-regulated gene products in K562. GA treatment downregulated the expression of SRC-3 and then inhibited the activity of Akt kinase and its downstream targets p70 S6 kinase 1 (S6K1) and glycogen synthase kinase 3β (GSK3β) without changes in total protein levels of these three proteins, which thus influenced the expression of the apoptosis related gene Bcl-2 in K562 cells. These results suggest that GA might exhibit its strong antitumor effects via the interruption of SRC-3. © 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.subjectChemicals And Cas Registry Numbersen_HK
dc.titleGambogic acid induces G0/G1 arrest and apoptosis involving inhibition of SRC-3 and inactivation of Akt pathway in K562 leukemia 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.doi10.1016/j.tox.2009.04.059en_HK
dc.identifier.pmid19433130-
dc.identifier.scopuseid_2-s2.0-67649995348en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67649995348&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume262en_HK
dc.identifier.issue2en_HK
dc.identifier.spage98en_HK
dc.identifier.epage105en_HK
dc.identifier.isiWOS:000268941500002-
dc.identifier.citeulike4993576-

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