Loss of Mel-18 enhances breast cancer stem cell activity and tumorigenicity through activating Notch signaling mediated by the Wnt/TCF pathway

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dc.contributor.authorH Y Won-
dc.contributor.authorJ Y Lee-
dc.contributor.authorD H Shin-
dc.contributor.authorJ H Park-
dc.contributor.authorJ S Nam-
dc.contributor.authorHyoung-Chin Kim-
dc.contributor.authorG Kong-
dc.date.accessioned2017-04-19T09:35:54Z-
dc.date.available2017-04-19T09:35:54Z-
dc.date.issued2012-
dc.identifier.issn08926638-
dc.identifier.uri10.1096/fj.12-209247ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11086-
dc.description.abstractMel-18 has been proposed as a negative regulator of Bmi-1, a cancer stem cell (CSC) marker, but it is still unclear whether Mel-18 is involved in CSC regulation. Here, we examined the effect of Mel-18 on the stemness of human breast CSCs. In Mel-18 small hairpin RNA (shRNA)-transduced MCF-7 cells, side population (SP) cells and breast CSC surface marker (CD44+/CD24 -/ESA+)-expressing cells, which imply a CSC population, were enriched. Moreover, the self-renewal of CSCs was enhanced by Mel-18 knockdown, as measured by the ability for tumorsphere formation in vitro and tumor-initiating capacity in vivo. Similarly, Mel-18 overexpression inhibited the number and self-renewal activity of breast CSCs in SK-BR-3 cells. Furthermore, our data showed that Mel-18 blockade upregulated the expression of the Wnt/TCF target Jagged-1, a Notch ligand, and consequently activated the Notch pathway. Pharmacologic inhibition of the Notch and Wnt pathways abrogated Mel-18 knockdown-mediated tumorsphere formation ability. Taken together, our findings suggest that Mel-18 is a novel negative regulator of breast CSCs that inhibits the stem cell population and in vitro and in vivo self-renewal through the inactivation of Wnt-mediated Notch signaling.-
dc.publisherWiley-
dc.titleLoss of Mel-18 enhances breast cancer stem cell activity and tumorigenicity through activating Notch signaling mediated by the Wnt/TCF pathway-
dc.title.alternativeLoss of Mel-18 enhances breast cancer stem cell activity and tumorigenicity through activating Notch signaling mediated by the Wnt/TCF pathway-
dc.typeArticle-
dc.citation.titleFASEB Journal-
dc.citation.number12-
dc.citation.endPage5013-
dc.citation.startPage5002-
dc.citation.volume26-
dc.contributor.affiliatedAuthorHyoung-Chin Kim-
dc.contributor.alternativeName원희영-
dc.contributor.alternativeName이정연-
dc.contributor.alternativeName신동희-
dc.contributor.alternativeName박지혜-
dc.contributor.alternativeName남정석-
dc.contributor.alternativeName김형진-
dc.contributor.alternativeName공구-
dc.identifier.bibliographicCitationFASEB Journal, vol. 26, no. 12, pp. 5002-5013-
dc.identifier.doi10.1096/fj.12-209247-
dc.subject.keywordJagged-1-
dc.subject.keywordPolycomb-
dc.subject.keywordSelf-renewal-
dc.subject.keywordStemness-
dc.subject.localJagged-1-
dc.subject.localPolycomb-
dc.subject.localSelf-renewal-
dc.subject.localStemness-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of Bioinfrastructure > 1. Journal Articles
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