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Human arrest defective 1 acetylates and activates beta-catenin, promoting lung cancer cell proliferation

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dc.contributor.authorLim, J. H.-
dc.contributor.authorPark, J. W.-
dc.contributor.authorChun, Y. S.-
dc.date.accessioned2009-12-29T02:09:28Z-
dc.date.available2009-12-29T02:09:28Z-
dc.date.issued2006-11-17-
dc.identifier.citationCancer Res. 2006 Nov 15;66(22):10677-82.en
dc.identifier.issn0008-5472 (Print)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17108104-
dc.identifier.urihttps://hdl.handle.net/10371/22955-
dc.description.abstractArrest defective 1 (ARD1), an acetyltransferase, is essential for the yeast life cycle. Although its human homologue (hARD1) has been identified, its biological functions in human cells remain unclear. In the present study, we examined the biological function of hARD1. In H1299 and A549 lung cancer cells, hARD1-silencing RNA inhibited cell proliferation and induced G(1) arrest. Cyclin D1 was also found to be down-regulated in these growth-arrested cells, and the ectopic expression of cyclin D1 rescued cell growth. hARD1 knockdown repressed the promoter activity of the cyclin D1 gene, which inhibited the transcription of cyclin D1. Moreover, hARD1 knockdown reduced the binding of beta-catenin/TCF4 transcription factor to cyclin D1 promoter and repressed its transcriptional activity. Inversely, hARD1 expression increased the transcriptional activity of beta-catenin. Both endogenous and ectopically expressed hARD1 was coimmunoprecipitated with beta-catenin. hARD1 knockdown did not affect beta-catenin expression or degradation but noticeably reduced acetylated beta-catenin. The beta-catenin binding and acetylation by hARD1 were observed in vitro. Therefore, it is suggested that hARD1 participates in proliferation of lung cancer cells via the activation of beta-catenin.en
dc.language.isoen-
dc.publisherAmerican Association for Cancer Researchen
dc.subjectAcetylationen
dc.subjectAcetyltransferases/genetics/*metabolismen
dc.subjectCarcinoma, Non-Small-Cell Lung/enzymology/*metabolism/pathologyen
dc.subjectCell Growth Processes/physiologyen
dc.subjectCell Line, Tumoren
dc.subjectCyclin D1/genetics/metabolismen
dc.subjectG1 Phase/physiologyen
dc.subjectHumansen
dc.subjectLung Neoplasms/enzymology/*metabolism/pathologyen
dc.subjectPromoter Regions, Geneticen
dc.subjectProtein Bindingen
dc.subjectRNA, Small Interfering/geneticsen
dc.subjectTCF Transcription Factors/metabolismen
dc.subjectbeta Catenin/antagonists & inhibitors/genetics/*metabolismen
dc.titleHuman arrest defective 1 acetylates and activates beta-catenin, promoting lung cancer cell proliferationen
dc.typeArticleen
dc.contributor.AlternativeAuthor임지홍-
dc.contributor.AlternativeAuthor박종완-
dc.contributor.AlternativeAuthor전양숙-
dc.identifier.doi10.1158/0008-5472.CAN-06-3171-
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