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Article: Wortmannin inhibits K562 lukemic cells by regulating PI3k/Akt channel in vitro

TitleWortmannin inhibits K562 lukemic cells by regulating PI3k/Akt channel in vitro
Authors
KeywordsIkk-Κb
K562 Cell
Nf-Κb
P-Akt
Wortmannin
Issue Date2009
Citation
Journal of Huazhong University of Science and Technology - Medical Science, 2009, v. 29 n. 4, p. 451-456 How to Cite?
AbstractThe inhibitory effect of wortmannin on leukemic cells and the possible mechanisms were examined. K562 cells were treated with wortmannin of various concentrations (3.125-100 nmol/L) for 0-72 h. MTT assay was used to evaluate the inhibitory effect of wortmannin on the growth of K562 cells. Cell apoptosis was detected by both Annexin-V FITC/PI double-labeled cytometry and transmission electron microscopy (TEM). The expression of p-Akt, T-p-Akt, NF-κBp65 and IKK-κB was determined by Western blotting and reverse transcription- polymerase chain reaction (RT-PCR). Our results showed that wortmannin obviously inhibited growth and induced apoptosis of K562 cells in vitro in a time- and dose-dependent manner. The IC50 value of wortmannin for 24 h was 25±0.14 nmol/L. Moreover, wortmannin induced K562 cells apoptosis in a dose-dependent manner. TEM revealed typical morphological changes of apoptosis in wortmannin-treated K562 cells, such as chromatin condensation, karyopyknosis, karyorhexis and apoptotic bodies. Additionally, several important intracellular protein kinases such as p-Akt, NF-κBp65 and IKK-κB experienced degradation of various degrees in a dose-dependent manner both at protein level and transcription level when cultured with wortmannin, but the expression of total Akt showed no change. It is concluded that wortmannin can inhibit the proliferation and induce apoptosis of K562 leukemia cells possibly by down-regulating the survival signaling pathways (PI3K/Akt and NF-κB channels). © 2009 Huazhong University of Science and Technology and Springer-Verlag GmbH.
Persistent Identifierhttp://hdl.handle.net/10722/92345
ISSN
2015 Impact Factor: 0.838
2015 SCImago Journal Rankings: 0.344
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Sciences Foundation of China30671743
Funding Information:

This project was supported by a grant from the National Natural Sciences Foundation of China (No. 30671743).

References

 

DC FieldValueLanguage
dc.contributor.authorWu, Qen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorCui, Gen_HK
dc.contributor.authorCheng, Yen_HK
dc.date.accessioned2010-09-17T10:43:19Z-
dc.date.available2010-09-17T10:43:19Z-
dc.date.issued2009en_HK
dc.identifier.citationJournal of Huazhong University of Science and Technology - Medical Science, 2009, v. 29 n. 4, p. 451-456en_HK
dc.identifier.issn1672-0733en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92345-
dc.description.abstractThe inhibitory effect of wortmannin on leukemic cells and the possible mechanisms were examined. K562 cells were treated with wortmannin of various concentrations (3.125-100 nmol/L) for 0-72 h. MTT assay was used to evaluate the inhibitory effect of wortmannin on the growth of K562 cells. Cell apoptosis was detected by both Annexin-V FITC/PI double-labeled cytometry and transmission electron microscopy (TEM). The expression of p-Akt, T-p-Akt, NF-κBp65 and IKK-κB was determined by Western blotting and reverse transcription- polymerase chain reaction (RT-PCR). Our results showed that wortmannin obviously inhibited growth and induced apoptosis of K562 cells in vitro in a time- and dose-dependent manner. The IC50 value of wortmannin for 24 h was 25±0.14 nmol/L. Moreover, wortmannin induced K562 cells apoptosis in a dose-dependent manner. TEM revealed typical morphological changes of apoptosis in wortmannin-treated K562 cells, such as chromatin condensation, karyopyknosis, karyorhexis and apoptotic bodies. Additionally, several important intracellular protein kinases such as p-Akt, NF-κBp65 and IKK-κB experienced degradation of various degrees in a dose-dependent manner both at protein level and transcription level when cultured with wortmannin, but the expression of total Akt showed no change. It is concluded that wortmannin can inhibit the proliferation and induce apoptosis of K562 leukemia cells possibly by down-regulating the survival signaling pathways (PI3K/Akt and NF-κB channels). © 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.subjectIkk-Κben_HK
dc.subjectK562 Cellen_HK
dc.subjectNf-Κben_HK
dc.subjectP-Akten_HK
dc.subjectWortmanninen_HK
dc.titleWortmannin inhibits K562 lukemic cells by regulating PI3k/Akt channel 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/s11596-009-0412-xen_HK
dc.identifier.pmid19662361-
dc.identifier.scopuseid_2-s2.0-68949132404en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-68949132404&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume29en_HK
dc.identifier.issue4en_HK
dc.identifier.spage451en_HK
dc.identifier.epage456en_HK
dc.identifier.isiWOS:000268772600012-
dc.identifier.citeulike5427377-

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