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Article: Deguelin blocks cells survival signal pathways and induces apoptosis of HL-60 cells in vitro

TitleDeguelin blocks cells survival signal pathways and induces apoptosis of HL-60 cells in vitro
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2009
PublisherSpringer Japan KK
Citation
International Journal of Hematology, 2009, v. 89 n. 5, p. 618-623 How to Cite?
AbstractTo investigate the anti-cancer effects and molecular mechanism of deguelin on the human leukemia HL-60 cells, to explore the expression and clinical significance of p-AKT, survivin and Bcl-2 in leukemia cell line HL-60 cell. Cell growth rate was assessed by MTT assay. Apoptotic index was evaluated by TUNEL staining. Apoptosis was detected by Annexin V-FITC Apoptosis Detection Kit and transmission electron microscopy (TEM), expression of p-Akt, Bcl-2 and surviving in HL-60 cells was checked by Western blot. Deguelin presented striking proliferation inhibition potency on HL-60 cells in vitro, with the I C50 value for 48 h being 20.14 nM, and induced apoptosis in HL-60 in a concentration-time-dependent manner. Apoptotic bodies and cell shrinkage and fragmentation were observed by TUNEL and TEM. Deguelin-induced cells morphological changes and degraded several kinase proteins, including Bcl-2 and survivin (members of lap). The degradation of these kinases blocked PI3K/Akt survival signal pathways, inducing apoptosis. Deguelin may induce HL-60 cell apoptosis through depletion of multiple kinase proteins and blockage of survival signal pathways of HL-60 cells. © 2009 The Japanese Society of Hematology.
Persistent Identifierhttp://hdl.handle.net/10722/92268
ISSN
2015 Impact Factor: 1.846
2015 SCImago Journal Rankings: 0.779
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Sciences Foundation of China30472268
Institute of Occupational Medicine
Tongji Medical College
Huazhong University of Science and Technology, Wuhan, China
Funding Information:

This work was supported by a grant from the National Natural Sciences Foundation of China ( No. 30472268). It was supported in part by the Institute of Occupational Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. We thank Dr. Tang-chun Wu, Dr. Mei-an He, Dr. Chang-zhen Jiang and Dr. Hao Tang for helpful experiment assistance.

References

 

DC FieldValueLanguage
dc.contributor.authorChen, Yen_HK
dc.contributor.authorWu, Qen_HK
dc.contributor.authorCui, G-Hen_HK
dc.contributor.authorChen, Y-Qen_HK
dc.contributor.authorLi, Ren_HK
dc.date.accessioned2010-09-17T10:41:01Z-
dc.date.available2010-09-17T10:41:01Z-
dc.date.issued2009en_HK
dc.identifier.citationInternational Journal of Hematology, 2009, v. 89 n. 5, p. 618-623en_HK
dc.identifier.issn0925-5710en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92268-
dc.description.abstractTo investigate the anti-cancer effects and molecular mechanism of deguelin on the human leukemia HL-60 cells, to explore the expression and clinical significance of p-AKT, survivin and Bcl-2 in leukemia cell line HL-60 cell. Cell growth rate was assessed by MTT assay. Apoptotic index was evaluated by TUNEL staining. Apoptosis was detected by Annexin V-FITC Apoptosis Detection Kit and transmission electron microscopy (TEM), expression of p-Akt, Bcl-2 and surviving in HL-60 cells was checked by Western blot. Deguelin presented striking proliferation inhibition potency on HL-60 cells in vitro, with the I C50 value for 48 h being 20.14 nM, and induced apoptosis in HL-60 in a concentration-time-dependent manner. Apoptotic bodies and cell shrinkage and fragmentation were observed by TUNEL and TEM. Deguelin-induced cells morphological changes and degraded several kinase proteins, including Bcl-2 and survivin (members of lap). The degradation of these kinases blocked PI3K/Akt survival signal pathways, inducing apoptosis. Deguelin may induce HL-60 cell apoptosis through depletion of multiple kinase proteins and blockage of survival signal pathways of HL-60 cells. © 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.titleDeguelin blocks cells survival signal pathways and induces apoptosis of HL-60 cells 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.doi10.1007/s12185-009-0307-4en_HK
dc.identifier.pmid19455392-
dc.identifier.scopuseid_2-s2.0-67749109791en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-67749109791&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume89en_HK
dc.identifier.issue5en_HK
dc.identifier.spage618en_HK
dc.identifier.epage623en_HK
dc.identifier.isiWOS:000266583200009-
dc.identifier.citeulike4607540-

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