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Snail reprograms glucose metabolism by repressing phosphofructokinase PFKP allowing cancer cell survival under metabolic stress

DC Field Value Language
dc.contributor.author김현실-
dc.contributor.author류주경-
dc.contributor.author양지혜-
dc.contributor.author육종인-
dc.contributor.author차소영-
dc.contributor.author차용훈-
dc.contributor.author정재호-
dc.contributor.author김남희-
dc.contributor.author이윤미-
dc.contributor.author장향란-
dc.contributor.author조은애-
dc.date.accessioned2017-11-01T08:43:51Z-
dc.date.available2017-11-01T08:43:51Z-
dc.date.issued2017-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/153577-
dc.description.abstractDynamic regulation of glucose flux between aerobic glycolysis and the pentose phosphate pathway (PPP) during epithelial-mesenchymal transition (EMT) is not well-understood. Here we show that Snail (SNAI1), a key transcriptional repressor of EMT, regulates glucose flux toward PPP, allowing cancer cell survival under metabolic stress. Mechanistically, Snail regulates glycolytic activity via repression of phosphofructokinase, platelet (PFKP), a major isoform of cancer-specific phosphofructokinase-1 (PFK-1), an enzyme involving the first rate-limiting step of glycolysis. The suppression of PFKP switches the glucose flux towards PPP, generating NADPH with increased metabolites of oxidative PPP. Functionally, dynamic regulation of PFKP significantly potentiates cancer cell survival under metabolic stress and increases metastatic capacities in vivo. Further, knockdown of PFKP rescues metabolic reprogramming and cell death induced by loss of Snail. Thus, the Snail-PFKP axis plays an important role in cancer cell survival via regulation of glucose flux between glycolysis and PPP.-
dc.description.statementOfResponsibilityopen-
dc.formatapplication/pdf-
dc.languageEnglish-
dc.publisherNature Pub. Group-
dc.relation.isPartOfNATURE COMMUNICATIONS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleSnail reprograms glucose metabolism by repressing phosphofructokinase PFKP allowing cancer cell survival under metabolic stress-
dc.typeArticle-
dc.publisher.locationEngland-
dc.contributor.collegeCollege of Dentistry-
dc.contributor.departmentDept. of Oral Pathology-
dc.contributor.googleauthorNam Hee Kim-
dc.contributor.googleauthorYong Hoon Cha-
dc.contributor.googleauthorJueun Lee-
dc.contributor.googleauthorSeon-Hyeong Lee-
dc.contributor.googleauthorJi Hye Yang-
dc.contributor.googleauthorJun Seop Yun-
dc.contributor.googleauthorEunae Sandra Cho-
dc.contributor.googleauthorXianglan Zhang-
dc.contributor.googleauthorMiso Nam-
dc.contributor.googleauthorNami Kim-
dc.contributor.googleauthorYoung-Su Yuk-
dc.contributor.googleauthorSo Young Cha-
dc.contributor.googleauthorYoonmi Lee-
dc.contributor.googleauthorJoo Kyung Ryu-
dc.contributor.googleauthorSunghyouk Park-
dc.contributor.googleauthorJae-Ho Cheong-
dc.contributor.googleauthorSang Won Kang-
dc.contributor.googleauthorSoo-Youl Kim-
dc.contributor.googleauthorGeum-Sook Hwang-
dc.contributor.googleauthorJong In Yook-
dc.contributor.googleauthorHyun Sil Kim-
dc.identifier.doi10.1038/ncomms14374-
dc.contributor.localIdA05123-
dc.contributor.localIdA05149-
dc.contributor.localIdA02536-
dc.contributor.localIdA03997-
dc.contributor.localIdA04000-
dc.contributor.localIdA03717-
dc.contributor.localIdA00360-
dc.contributor.localIdA03019-
dc.contributor.localIdA03489-
dc.contributor.localIdA01121-
dc.relation.journalcodeJ02293-
dc.identifier.eissn2041-1723-
dc.identifier.pmid28176759-
dc.contributor.alternativeNameKim, Hyun Sil-
dc.contributor.alternativeNameRyu, Joo Kyung-
dc.contributor.alternativeNameYang, Ji Hye-
dc.contributor.alternativeNameYook, Jong In-
dc.contributor.alternativeNameCha, So Young-
dc.contributor.alternativeNameCha, Yong Hoon-
dc.contributor.alternativeNameCheong, Jae Ho-
dc.contributor.alternativeNameKim, Nam Hee-
dc.contributor.alternativeNameLee, Yoon Mi-
dc.contributor.alternativeNameZhang, Xiang Lan-
dc.contributor.affiliatedAuthorRyu, Joo Kyung-
dc.contributor.affiliatedAuthorYang, Ji Hye-
dc.contributor.affiliatedAuthorYook, Jong In-
dc.contributor.affiliatedAuthorCha, So Young-
dc.contributor.affiliatedAuthorCha, Yong Hoon-
dc.contributor.affiliatedAuthorCheong, Jae Ho-
dc.contributor.affiliatedAuthorKim, Nam Hee-
dc.contributor.affiliatedAuthorLee, Yoon Mi-
dc.contributor.affiliatedAuthorZhang, Xiang Lan-
dc.contributor.affiliatedAuthorKim, Hyun Sil-
dc.citation.titleNature Communications-
dc.citation.volume8-
dc.citation.startPage14374-
dc.identifier.bibliographicCitationNATURE COMMUNICATIONS, Vol.8 : 14374, 2017-
dc.date.modified2017-11-01-
dc.identifier.rimsid42277-
dc.type.rimsART-
Appears in Collections:
2. College of Dentistry (치과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 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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