Cited 35 times in
Metabolic stress induces a Wnt-dependent cancer stem cell-like state transition
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이유진 | - |
dc.contributor.author | 정재호 | - |
dc.contributor.author | 허용민 | - |
dc.contributor.author | 구민희 | - |
dc.contributor.author | 김남희 | - |
dc.contributor.author | 박은성 | - |
dc.contributor.author | 서진석 | - |
dc.contributor.author | 양재문 | - |
dc.contributor.author | 육종인 | - |
dc.date.accessioned | 2016-02-04T11:36:42Z | - |
dc.date.available | 2016-02-04T11:36:42Z | - |
dc.date.issued | 2015 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/140808 | - |
dc.description.abstract | Reciprocal interactions between cancer cells and the tumor microenvironment drive multiple clinically significant behaviors including dormancy, invasion, and metastasis as well as therapy resistance. These microenvironment-dependent phenotypes share typical characteristics with cancer stem cells (CSC). However, it is poorly understood how metabolic stress in the confined tumor microenvironment contributes to the emergence and maintenance of CSC-like phenotypes. Here, we demonstrate that chronic metabolic stress (CMS) in a long-term nutrient deprivation induces a Wnt-dependent phenoconversion of non-stem cancer cells toward stem-like state and this is reflected in the transcriptome analysis. Addition of Wnt3a as well as transfection of dominant-negative Tcf4 establishes an obligatory role for the Wnt pathway in the acquisition of CSC-like characteristics in response to metabolic stress. Furthermore, systematic characterization for multiple single cell-derived clones and negative enrichment of CD44+/ESA+ stem-like cancer cells, all of which recapitulate stem-like cancer characteristics, suggest stochastic adaptation rather than selection of pre-existing subclones. Finally, CMS in the tumor microenvironment can drive a CSC-like phenoconversion of non-stem cancer cells through stochastic state transition dependent on the Wnt pathway. These findings contribute to an understanding of the metabolic stress-driven dynamic transition of non-stem cancer cells to a stem-like state in the tumor metabolic microenvironment. | - |
dc.description.statementOfResponsibility | open | - |
dc.format | application/pdf | - |
dc.relation.isPartOf | CELL DEATH & DISEASE | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Breast Neoplasms/pathology* | - |
dc.subject.MESH | Cell Proliferation | - |
dc.subject.MESH | Cell Survival | - |
dc.subject.MESH | Female | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Mice, Inbred BALB C | - |
dc.subject.MESH | Mice, Nude | - |
dc.subject.MESH | Neoplastic Stem Cells/cytology* | - |
dc.subject.MESH | Neoplastic Stem Cells/pathology | - |
dc.subject.MESH | Spheroids, Cellular/pathology | - |
dc.subject.MESH | Stress, Physiological/physiology* | - |
dc.subject.MESH | Transcription, Genetic/genetics | - |
dc.subject.MESH | Transcriptional Activation/genetics | - |
dc.subject.MESH | Tumor Cells, Cultured | - |
dc.subject.MESH | Tumor Microenvironment/physiology | - |
dc.subject.MESH | Wnt Signaling Pathway/physiology* | - |
dc.subject.MESH | Wnt3A Protein/metabolism* | - |
dc.subject.MESH | Xenograft Model Antitumor Assays | - |
dc.title | Metabolic stress induces a Wnt-dependent cancer stem cell-like state transition | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Surgery (외과학) | - |
dc.contributor.googleauthor | E Lee | - |
dc.contributor.googleauthor | J Yang | - |
dc.contributor.googleauthor | M Ku | - |
dc.contributor.googleauthor | NH Kim | - |
dc.contributor.googleauthor | Y Park | - |
dc.contributor.googleauthor | CB Park | - |
dc.contributor.googleauthor | J-S Suh | - |
dc.contributor.googleauthor | ES Park | - |
dc.contributor.googleauthor | JI Yook | - |
dc.contributor.googleauthor | GB Mills | - |
dc.contributor.googleauthor | Y-M Huh | - |
dc.contributor.googleauthor | J-H Cheong | - |
dc.identifier.doi | 10.1038/cddis.2015.171 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A03016 | - |
dc.contributor.localId | A03717 | - |
dc.contributor.localId | A04359 | - |
dc.contributor.localId | A00191 | - |
dc.contributor.localId | A00360 | - |
dc.contributor.localId | A01609 | - |
dc.contributor.localId | A01916 | - |
dc.contributor.localId | A02536 | - |
dc.contributor.localId | A02315 | - |
dc.relation.journalcode | J00482 | - |
dc.identifier.eissn | 2041-4889 | - |
dc.identifier.pmid | 26136078 | - |
dc.contributor.alternativeName | Lee, Eu Gene | - |
dc.contributor.alternativeName | Cheong, Jae Ho | - |
dc.contributor.alternativeName | Huh, Yong Min | - |
dc.contributor.alternativeName | Ku, Min Hee | - |
dc.contributor.alternativeName | Kim, Nam Hee | - |
dc.contributor.alternativeName | Park, Eun Sung | - |
dc.contributor.alternativeName | Suh, Jin Suck | - |
dc.contributor.alternativeName | Yang, Jae Moon | - |
dc.contributor.alternativeName | Yook, Jong In | - |
dc.contributor.affiliatedAuthor | Lee, Eu Gene | - |
dc.contributor.affiliatedAuthor | Cheong, Jae Ho | - |
dc.contributor.affiliatedAuthor | Huh, Yong Min | - |
dc.contributor.affiliatedAuthor | Ku, Min Hee | - |
dc.contributor.affiliatedAuthor | Kim, Nam Hee | - |
dc.contributor.affiliatedAuthor | Park, Eun Sung | - |
dc.contributor.affiliatedAuthor | Suh, Jin Suck | - |
dc.contributor.affiliatedAuthor | Yook, Jong In | - |
dc.contributor.affiliatedAuthor | Yang, Jae Moon | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 6 | - |
dc.citation.startPage | 1805 | - |
dc.identifier.bibliographicCitation | CELL DEATH & DISEASE, Vol.6 : 1805, 2015 | - |
dc.identifier.rimsid | 30321 | - |
dc.type.rims | ART | - |
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