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Metastasis-associated protein 1 enhances stability of hypoxia-inducible factor-1 alpha protein by recruiting histone deacetylase 1

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dc.contributor.authorYoo, Young-Gun-
dc.contributor.authorKong, Gu-
dc.contributor.authorLee, Mi-Ock-
dc.date.accessioned2022-12-21T11:56:33Z-
dc.date.available2022-12-21T11:56:33Z-
dc.date.created2022-08-26-
dc.date.issued2006-03-
dc.identifier.issn0261-4189-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/181734-
dc.description.abstractThe expression of metastasis-associated protein 1 (MTA1) correlates well with tumor metastases; however, the associated molecular mechanism is not fully understood. Here, we explored the possibility of cross-talk between MTA1 and hypoxia-inducible factor-1 alpha (HIF-1 alpha), a key regulator of angiogenic factors. We observed that the expression of MTA1 was strongly induced under hypoxia in breast cancer cell lines such as MCF-7 and MDA-MB-231. When MTA1 was overexpressed, the transcriptional activity and stability of HIF-1 alpha protein were enhanced. MTA1 and HIF-1 alpha are physically associated in vivo and they were localized completely in the nucleus when coexpressed. MTA1 induced the deacetylation of HIF-1 alpha by increasing the expression of histone deacetylase 1 (HDAC1). MTA1 counteracted to the action of acetyltransferase, ARD1, and it did not stabilize the HIF-1 alpha mutant that lacks the acetylation site, K532R. These results indicate that acetylation is the major target of MTA1/HDAC1 function. Collectively, our data provide evidence of a positive cross-talk between HIF-1 alpha and MTA1, which is mediated by HDAC1 recruitment, and indicate a close connection between MTA1-associated metastasis and HIF-1-induced tumor angiogenesis.-
dc.language영어-
dc.language.isoen-
dc.publisherWILEY-
dc.titleMetastasis-associated protein 1 enhances stability of hypoxia-inducible factor-1 alpha protein by recruiting histone deacetylase 1-
dc.typeArticle-
dc.contributor.affiliatedAuthorKong, Gu-
dc.identifier.doi10.1038/sj.emboj.7601025-
dc.identifier.scopusid2-s2.0-33645322383-
dc.identifier.wosid000236737700006-
dc.identifier.bibliographicCitationEMBO JOURNAL, v.25, no.6, pp.1231 - 1241-
dc.relation.isPartOfEMBO JOURNAL-
dc.citation.titleEMBO JOURNAL-
dc.citation.volume25-
dc.citation.number6-
dc.citation.startPage1231-
dc.citation.endPage1241-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaCell Biology-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryCell Biology-
dc.subject.keywordPlusHYPOXIA-INDUCIBLE FACTOR-1-ALPHA-
dc.subject.keywordPlusVIRUS-X PROTEIN-
dc.subject.keywordPlusHUMAN MTA1 GENE-
dc.subject.keywordPlusBREAST-CANCER-
dc.subject.keywordPlusESTROGEN-RECEPTOR-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusALPHA-
dc.subject.keywordPlusOVEREXPRESSION-
dc.subject.keywordPlusHIF-1-ALPHA-
dc.subject.keywordPlusFAMILY-
dc.subject.keywordAuthorHDAC1-
dc.subject.keywordAuthorHIF-1 alpha-
dc.subject.keywordAuthorhypoxia-
dc.subject.keywordAuthormetastasis-
dc.subject.keywordAuthorMTA1-
dc.identifier.urlhttps://www.embopress.org/doi/full/10.1038/sj.emboj.7601025-
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