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Article: Involvement of SRC-3 in deguelin-induced apoptosis in Jurkat cells

TitleInvolvement of SRC-3 in deguelin-induced apoptosis in Jurkat cells
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2009
PublisherSpringer Japan KK
Citation
International Journal of Hematology, 2009, v. 89 n. 5, p. 628-635 How to Cite?
AbstractThe aim of the study was to investigate the anticancer effects and the molecular mechanisms of deguelin on Jurkat cells. Cell viability was assessed by MTT assay. Terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) assay and transmission electron microscopy were used to detect cell apoptosis. A propidium iodide method was used to study cell cycle distribution. RT-PCR and Western blotting were employed to assess the expression levels of steroid receptor coactivator-3 (SRC-3), nuclear factor-κB (NF-κB) and some apoptosis related genes, including Bcl-2 and Bcl-xL. Deguelin was able to inhibit cell proliferation by a cell-cycle arrest in the G1/G 0 phase and induce apoptosis in Jurkat cells in vitro, with a 24-h IC50 value of 43.73 ± 0.35 nmol/L. The antileukemia effect of deguelin might be correlated well with the downregulation of the expression of SRC-3 and its related transcription factor NF-κB, which thus influenced the expression of apoptosis related genes Bcl-2 and Bcl-xL. Deguelin presented potent effects on growth arrest and apoptosis induction in Jurkat cells in vitro via the interruption of SRC-3. © 2009 The Japanese Society of Hematology.
Persistent Identifierhttp://hdl.handle.net/10722/92196
ISSN
2015 Impact Factor: 1.846
2015 SCImago Journal Rankings: 0.779
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 Immunology, 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.authorShu, W-Xen_HK
dc.contributor.authorChen, Zen_HK
dc.contributor.authorKe, W-Jen_HK
dc.date.accessioned2010-09-17T10:38:54Z-
dc.date.available2010-09-17T10:38:54Z-
dc.date.issued2009en_HK
dc.identifier.citationInternational Journal of Hematology, 2009, v. 89 n. 5, p. 628-635en_HK
dc.identifier.issn0925-5710en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92196-
dc.description.abstractThe aim of the study was to investigate the anticancer effects and the molecular mechanisms of deguelin on Jurkat cells. Cell viability was assessed by MTT assay. Terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) assay and transmission electron microscopy were used to detect cell apoptosis. A propidium iodide method was used to study cell cycle distribution. RT-PCR and Western blotting were employed to assess the expression levels of steroid receptor coactivator-3 (SRC-3), nuclear factor-κB (NF-κB) and some apoptosis related genes, including Bcl-2 and Bcl-xL. Deguelin was able to inhibit cell proliferation by a cell-cycle arrest in the G1/G 0 phase and induce apoptosis in Jurkat cells in vitro, with a 24-h IC50 value of 43.73 ± 0.35 nmol/L. The antileukemia effect of deguelin might be correlated well with the downregulation of the expression of SRC-3 and its related transcription factor NF-κB, which thus influenced the expression of apoptosis related genes Bcl-2 and Bcl-xL. Deguelin presented potent effects on growth arrest and apoptosis induction in Jurkat cells in vitro via the interruption of SRC-3. © 2009 The Japanese Society of Hematology.en_HK
dc.languageengen_HK
dc.publisherSpringer Japan KKen_HK
dc.relation.ispartofInternational Journal of Hematologyen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.titleInvolvement of SRC-3 in deguelin-induced apoptosis in Jurkat 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/s12185-009-0311-8en_HK
dc.identifier.pmid19365708-
dc.identifier.scopuseid_2-s2.0-67749107960en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67749107960&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume89en_HK
dc.identifier.issue5en_HK
dc.identifier.spage628en_HK
dc.identifier.epage635en_HK
dc.identifier.isiWOS:000266583200011-
dc.identifier.citeulike4341363-

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