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Cited 26 times in

Catabolic metabolism during cancer EMT

DC Field Value Language
dc.contributor.author김남희-
dc.contributor.author김현실-
dc.contributor.author육종인-
dc.contributor.author차용훈-
dc.date.accessioned2016-02-04T11:06:30Z-
dc.date.available2016-02-04T11:06:30Z-
dc.date.issued2015-
dc.identifier.issn0253-6269-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/139681-
dc.description.abstractAerobic glycolysis is widely accepted as the glucose metabolism for production of biomass such as nucleotides, amino acids, and fatty acids which underlie the anabolic process of cancer cell proliferation. The epithelial-mesenchymal transition (EMT) is a complex cellular mechanism for invasion and metastatic progression in cancer cells. While Snail-mediated EMT regulated by major oncogenic signaling has been well-studied over the last decade, metabolic reprogramming during the EMT has not. In this work, we emphasize the importance of catabolic metabolism for cancer cell survival during cancer cell EMT. Because specific catabolic processes such as autophage and fatty acid oxidation have been well explained, we mainly focus on the general aspects of energy metabolism promoting cancer cell survival under metabolic stress. We also revisit the role of mitochondria in catabolism as oxidative phosphorylation in cancer has long been underestimated. Considering the highly inefficient process of metastatic progression and profound metabolic stress following matrix detachment of solid cancer, catabolic reprogramming during the EMT may play an important role in overcoming metastatic inefficiency of cancer cells.-
dc.description.statementOfResponsibilityopen-
dc.format.extent313~320-
dc.relation.isPartOfARCHIVES OF PHARMACAL RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHCell Survival/physiology-
dc.subject.MESHEnergy Metabolism/physiology*-
dc.subject.MESHEpithelial-Mesenchymal Transition/physiology*-
dc.subject.MESHGlucose/metabolism-
dc.subject.MESHGlycolysis/physiology-
dc.subject.MESHHumans-
dc.subject.MESHMitochondria/metabolism-
dc.subject.MESHNeoplasm Metastasis-
dc.subject.MESHNeoplasms/metabolism*-
dc.subject.MESHNeoplasms/pathology-
dc.subject.MESHOxidative Phosphorylation-
dc.subject.MESHStress, Physiological/physiology-
dc.titleCatabolic metabolism during cancer EMT-
dc.typeArticle-
dc.contributor.collegeResearcher Institutes (부설 연구소)-
dc.contributor.departmentOral Cancer Research Institute (구강종양연구소)-
dc.contributor.googleauthorYong Hoon Cha-
dc.contributor.googleauthorJong In Yook-
dc.contributor.googleauthorHyun Sil Kim-
dc.contributor.googleauthorNam Hee Kim-
dc.identifier.doi10.1007/s12272-015-0567-x-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00360-
dc.contributor.localIdA01121-
dc.contributor.localIdA02536-
dc.contributor.localIdA04000-
dc.relation.journalcodeJ00229-
dc.identifier.pmid25634102-
dc.identifier.urlhttp://link.springer.com/article/10.1007%2Fs12272-015-0567-x-
dc.subject.keywordEpithelial–mesenchymal transition (EMT)-
dc.subject.keywordCatabolism-
dc.subject.keywordCancer-
dc.subject.keywordSurvival-
dc.contributor.alternativeNameKim, Nam Hee-
dc.contributor.alternativeNameKim, Hyun Sil-
dc.contributor.alternativeNameYook, Jong In-
dc.contributor.alternativeNameCha, Yong Hoon-
dc.contributor.affiliatedAuthorKim, Nam Hee-
dc.contributor.affiliatedAuthorKim, Hyun Sil-
dc.contributor.affiliatedAuthorYook, Jong In-
dc.contributor.affiliatedAuthorCha, Yong Hoon-
dc.rights.accessRightsnot free-
dc.citation.volume38-
dc.citation.number3-
dc.citation.startPage313-
dc.citation.endPage320-
dc.identifier.bibliographicCitationARCHIVES OF PHARMACAL RESEARCH, Vol.38(3) : 313-320, 2015-
dc.identifier.rimsid52401-
dc.type.rimsART-
Appears in Collections:
2. College of Dentistry (치과대학) > Research Institute (부설연구소) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Oral Pathology (구강병리학교실) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Oral and Maxillofacial Surgery (구강악안면외과학교실) > 1. Journal Papers

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