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Article: NGF inhibits human leukemia proliferation by downregulating cyclin A1 expression through promoting acinus/CtBP2 association

TitleNGF inhibits human leukemia proliferation by downregulating cyclin A1 expression through promoting acinus/CtBP2 association
Authors
KeywordsNGF
Cyclin A1
CtBP2
Acinus
Gambogic amide
Leukemia
Issue Date2009
Citation
Oncogene, 2009, v. 28, n. 43, p. 3825-3836 How to Cite?
AbstractCyclin A1 is essential for leukemia progression, and its expression is tightly regulated by acinus, a nuclear speckle protein. However, the molecular mechanism of how acinus mediates cyclin A1 expression remains elusive. Here we show that transcription corepressor CtBP2 directly binds acinus, which is regulated by nerve growth factor (NGF), inhibiting its stimulatory effect on cyclin A1, but not cyclin A2, expression in leukemia. NGF, a cognate ligand for the neurotrophic receptor TrkA, promotes the interaction between CtBP2 and acinus through triggering acinus phosphorylation by Akt. Overexpression of CtBP2 diminishes cyclin A1 transcription, whereas depletion of CtBP2 abolishes NGF's suppressive effect on cyclin A1 expression. Strikingly, gambogic amide, a newly identified TrkA agonist, potently represses cyclin A1 expression, thus blocking K562 cell proliferation. Moreover, gambogic amide ameliorates the leukemia progression in K562 cells inoculated nude mice. Hence, NGF downregulates cyclin A1 expression through escalating CtBP2/acinus complex formation, and gambogic amide might be useful for human leukemia treatment. © 2009 Macmillan Publishers Limited All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/225078
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047

 

DC FieldValueLanguage
dc.contributor.authorChan, C. B.-
dc.contributor.authorLiu, X.-
dc.contributor.authorJang, S. W.-
dc.contributor.authorHsu, S. I H-
dc.contributor.authorWilliams, I.-
dc.contributor.authorKang, S.-
dc.contributor.authorChen, J.-
dc.contributor.authorYe, K.-
dc.date.accessioned2016-04-18T11:16:43Z-
dc.date.available2016-04-18T11:16:43Z-
dc.date.issued2009-
dc.identifier.citationOncogene, 2009, v. 28, n. 43, p. 3825-3836-
dc.identifier.issn0950-9232-
dc.identifier.urihttp://hdl.handle.net/10722/225078-
dc.description.abstractCyclin A1 is essential for leukemia progression, and its expression is tightly regulated by acinus, a nuclear speckle protein. However, the molecular mechanism of how acinus mediates cyclin A1 expression remains elusive. Here we show that transcription corepressor CtBP2 directly binds acinus, which is regulated by nerve growth factor (NGF), inhibiting its stimulatory effect on cyclin A1, but not cyclin A2, expression in leukemia. NGF, a cognate ligand for the neurotrophic receptor TrkA, promotes the interaction between CtBP2 and acinus through triggering acinus phosphorylation by Akt. Overexpression of CtBP2 diminishes cyclin A1 transcription, whereas depletion of CtBP2 abolishes NGF's suppressive effect on cyclin A1 expression. Strikingly, gambogic amide, a newly identified TrkA agonist, potently represses cyclin A1 expression, thus blocking K562 cell proliferation. Moreover, gambogic amide ameliorates the leukemia progression in K562 cells inoculated nude mice. Hence, NGF downregulates cyclin A1 expression through escalating CtBP2/acinus complex formation, and gambogic amide might be useful for human leukemia treatment. © 2009 Macmillan Publishers Limited All rights reserved.-
dc.languageeng-
dc.relation.ispartofOncogene-
dc.subjectNGF-
dc.subjectCyclin A1-
dc.subjectCtBP2-
dc.subjectAcinus-
dc.subjectGambogic amide-
dc.subjectLeukemia-
dc.titleNGF inhibits human leukemia proliferation by downregulating cyclin A1 expression through promoting acinus/CtBP2 association-
dc.typeArticle-
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1038/onc.2009.236-
dc.identifier.pmid19668232-
dc.identifier.scopuseid_2-s2.0-70350700713-
dc.identifier.volume28-
dc.identifier.issue43-
dc.identifier.spage3825-
dc.identifier.epage3836-
dc.identifier.eissn1476-5594-

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