Cited 151 times in
Therapeutic implications of cancer epithelial-mesenchymal transition (EMT)
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김남희 | - |
dc.contributor.author | 육종인 | - |
dc.contributor.author | 조은애산드라 | - |
dc.date.accessioned | 2019-07-23T06:56:48Z | - |
dc.date.available | 2019-07-23T06:56:48Z | - |
dc.date.issued | 2019 | - |
dc.identifier.issn | 0253-6269 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/170389 | - |
dc.description.abstract | Theepithelial-mesenchymal transition(EMT) comprises an essential biological process involvingcancerprogression as well as initiation. While theEMThas been regarded as a phenotypic conversion fromepithelialtomesenchymalcells, recent evidence indicates that it plays a critical role in stemness, metabolic reprogramming, immune evasion andtherapeuticresistance ofcancercells. Interestingly, several transcriptional repressors including Snail (SNAI1), Slug (SNAI2) and the ZEB family constitute key players forEMTincanceras well as in the developmental process. Note that the dynamic conversion betweenEMTandepithelialreversion (mesenchymal-epithelialtransition, MET) occurs through variable intermediate-hybrid states rather than being a binary process. Given the close connection between oncogenic signaling andEMTrepressors, theEMThas emerged as atherapeutictarget or goal (in terms of MET reversion) incancertherapy. Here we review the critical role ofEMTintherapeuticresistance and the importance ofEMTas atherapeutictarget for humancancer. | - |
dc.description.statementOfResponsibility | restriction | - |
dc.language | English | - |
dc.publisher | Pharmaceutical Society of Korea | - |
dc.relation.isPartOf | ARCHIVES OF PHARMACAL RESEARCH | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Antineoplastic Agents/administration & dosage | - |
dc.subject.MESH | Antineoplastic Agents/metabolism | - |
dc.subject.MESH | Cell Line,Tumor | - |
dc.subject.MESH | Epithelial-Mesenchymal Transition/drug effects | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Neoplasms/drug therapy | - |
dc.subject.MESH | Neoplasms/metabolism | - |
dc.subject.MESH | Neoplasms/pathology | - |
dc.subject.MESH | Signal Transduction/drug effects | - |
dc.subject.MESH | Signal Transduction/physiology | - |
dc.subject.MESH | Transcription Factors/antagonists & inhibitors | - |
dc.subject.MESH | Transcription Factors/metabolism | - |
dc.title | Therapeutic implications of cancer epithelial-mesenchymal transition (EMT) | - |
dc.type | Article | - |
dc.contributor.college | Research Institutes (연구소) | - |
dc.contributor.department | Oral Cancer Research Institute (구강종양연구소) | - |
dc.contributor.googleauthor | Eunae Sandra Cho | - |
dc.contributor.googleauthor | Hee Eun Kang | - |
dc.contributor.googleauthor | Nam Hee Kim | - |
dc.contributor.googleauthor | Jong In Yook | - |
dc.identifier.doi | 10.1007/s12272-018-01108-7 | - |
dc.contributor.localId | A00360 | - |
dc.contributor.localId | A02536 | - |
dc.contributor.localId | A04799 | - |
dc.relation.journalcode | J00229 | - |
dc.identifier.pmid | 30649699 | - |
dc.identifier.url | https://link.springer.com/article/10.1007%2Fs12272-018-01108-7 | - |
dc.subject.keyword | EMT | - |
dc.subject.keyword | Epithelial-mesenchymal transition | - |
dc.subject.keyword | Oncogenes | - |
dc.subject.keyword | Snail | - |
dc.subject.keyword | Therapeuticresistance | - |
dc.subject.keyword | Wnt | - |
dc.contributor.alternativeName | Kim, Nam Hee | - |
dc.contributor.affiliatedAuthor | 김남희 | - |
dc.contributor.affiliatedAuthor | 육종인 | - |
dc.contributor.affiliatedAuthor | 조은애산드라 | - |
dc.citation.volume | 42 | - |
dc.citation.number | 1 | - |
dc.citation.startPage | 14 | - |
dc.citation.endPage | 24 | - |
dc.identifier.bibliographicCitation | ARCHIVES OF PHARMACAL RESEARCH, Vol.42(1) : 14-24, 2019 | - |
dc.identifier.rimsid | 62850 | - |
dc.type.rims | ART | - |
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