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Epigenetic regulation of long noncoding RNA UCA1 by SATB1 in breast cancer

DC Field Value Language
dc.contributor.author김미경-
dc.contributor.author김형표-
dc.contributor.author이종주-
dc.date.accessioned2018-01-23T05:52:25Z-
dc.date.available2018-01-23T05:52:25Z-
dc.date.issued2016-
dc.identifier.issn1976-6696-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/155754-
dc.description.abstractSpecial AT-rich sequence binding protein 1 (SATB1) is a nuclear matrix-associated DNA-binding protein that functions as a chromatin organizer. SATB1 is highly expressed in aggressive breast cancer cells and promotes growth and metastasis by reprograming gene expression. Through genomewide cross-examination of gene expression and histone methylation, we identified SATB1 target genes for which expression is associated with altered epigenetic marks. Among the identified genes, long noncoding RNA urothelial carcinoma-associated 1 (UCA1) was upregulated by SATB1 depletion. Upregulation of UCA1 coincided with increased H3K4 trimethylation (H3K4me3) levels and decreased H3K27 trimethylation (H3K27me3) levels. Our study showed that SATB1 binds to the upstream region of UCA1 in vivo, and that its promoter activity increases with SATB1 depletion. Furthermore, simultaneous depletion of SATB1 and UCA1 potentiated suppression of tumor growth and cell survival. Thus, SATB1 repressed the expression of oncogenic UCA1, suppressing growth and survival of breast cancer cells. [BMB Reports 2016; 49(10): 578-583].-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfBMB REPORTS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rightshttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleEpigenetic regulation of long noncoding RNA UCA1 by SATB1 in breast cancer-
dc.typeArticle-
dc.contributor.collegeOthers-
dc.contributor.departmentGangnam Severance Hospital-
dc.contributor.googleauthorJong-Joo Lee-
dc.contributor.googleauthorMikyoung Kim-
dc.contributor.googleauthorHyoung-Pyo Kim-
dc.identifier.doi10.5483/BMBRep.2016.49.10.156-
dc.contributor.localIdA05092-
dc.contributor.localIdA01163-
dc.contributor.localIdA03148-
dc.relation.journalcodeJ00348-
dc.identifier.eissn1976-670X-
dc.identifier.pmid27697109-
dc.contributor.alternativeNameKim, Mi Kyoung-
dc.contributor.alternativeNameKim, Hyoung Pyo-
dc.contributor.alternativeNameLee, Jong Joo-
dc.contributor.affiliatedAuthorKim, Mi Kyoung-
dc.contributor.affiliatedAuthorKim, Hyoung Pyo-
dc.contributor.affiliatedAuthorLee, Jong Joo-
dc.citation.volume49-
dc.citation.number10-
dc.citation.startPage578-
dc.citation.endPage583-
dc.identifier.bibliographicCitationBMB REPORTS, Vol.49(10) : 578-583, 2016-
dc.identifier.rimsid48208-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Tropica Medicine (열대의학교실) > 1. Journal Papers

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