Radiation driven epithelial-mesenchymal transition is mediated by Notch signaling in breast cancer
DC Field | Value | Language |
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dc.contributor.author | Kim, Rae-Kwon | - |
dc.contributor.author | Kaushik, Neha | - |
dc.contributor.author | Suh, Yongjoon | - |
dc.contributor.author | Yoo, Ki-Chun | - |
dc.contributor.author | Cui, Yan-Hong | - |
dc.contributor.author | Kim, Min-Jung | - |
dc.contributor.author | Lee, Hae-June | - |
dc.contributor.author | Kim, In-Gyu | - |
dc.contributor.author | Lee, Su-Jae | - |
dc.date.accessioned | 2021-08-02T16:29:18Z | - |
dc.date.available | 2021-08-02T16:29:18Z | - |
dc.date.created | 2021-05-12 | - |
dc.date.issued | 2016-08 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/22287 | - |
dc.description.abstract | Epithelial to mesenchymal transition (EMT) is developmental process associated with cancer metastasis. Here, we found that breast carcinoma cells adopt epithelial-to-mesenchymal transition (EMT) in response to fractionated-radiation. Importantly, we show that Notch signaling is highly activated in fractionally-irradiated tumors as compared to non-irradiated tumors that are accompanied by an EMT. Moreover, we uncovered the mechanism of Notch-driven EMT, in which Notch enhanced EMT through IL-6/JAK/STAT3 signaling axis in mammary tumor cells. Collectively, we present converging evidence from our studies that Notch2 is a critical mediator of radiation-induced EMT and responsible for induced malignant tumor growth. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | IMPACT JOURNALS LLC | - |
dc.title | Radiation driven epithelial-mesenchymal transition is mediated by Notch signaling in breast cancer | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Lee, Su-Jae | - |
dc.identifier.doi | 10.18632/oncotarget.10802 | - |
dc.identifier.scopusid | 2-s2.0-84982279839 | - |
dc.identifier.wosid | 000385433000063 | - |
dc.identifier.bibliographicCitation | ONCOTARGET, v.7, no.33, pp.53430 - 53442 | - |
dc.relation.isPartOf | ONCOTARGET | - |
dc.citation.title | ONCOTARGET | - |
dc.citation.volume | 7 | - |
dc.citation.number | 33 | - |
dc.citation.startPage | 53430 | - |
dc.citation.endPage | 53442 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalResearchArea | Cell Biology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.relation.journalWebOfScienceCategory | Cell Biology | - |
dc.subject.keywordPlus | GLIOMA-CELLS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | MIGRATION | - |
dc.subject.keywordPlus | PATHWAY | - |
dc.subject.keywordPlus | PROGRESSION | - |
dc.subject.keywordPlus | MECHANISMS | - |
dc.subject.keywordPlus | SLUG | - |
dc.subject.keywordAuthor | radiation | - |
dc.subject.keywordAuthor | EMT | - |
dc.subject.keywordAuthor | Notch signaling | - |
dc.subject.keywordAuthor | interleukin-6 | - |
dc.subject.keywordAuthor | breast cancer | - |
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