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Breast Cancer Subtypes Underlying EMT-Mediated Catabolic Metabolism

DC FieldValueLanguage
dc.contributor.author김남희-
dc.contributor.author김현실-
dc.contributor.author육종인-
dc.contributor.author조은애산드라-
dc.date.accessioned2020-12-01T16:44:11Z-
dc.date.available2020-12-01T16:44:11Z-
dc.date.issued2020-09-
dc.identifier.issn2073-4409-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/179951-
dc.description.abstractEfficient catabolic metabolism of adenosine triphosphate (ATP) and reduced nicotinamide adenine dinucleotide phosphate (NADPH) is essentially required for cancer cell survival, especially in metastatic cancer progression. Epithelial-mesenchymal transition (EMT) plays an important role in metabolic rewiring of cancer cells as well as in phenotypic conversion and therapeutic resistance. Snail (SNAI1), a well-known inducer of cancer EMT, is critical in providing ATP and NADPH via suppression of several gatekeeper genes involving catabolic metabolism, such as phosphofructokinase 1 (PFK1), fructose-1,6-bisphosphatase 1 (FBP1), and acetyl-CoA carboxylase 2 (ACC2). Paradoxically, PFK1 and FBP1 are counter-opposing and rate-limiting reaction enzymes of glycolysis and gluconeogenesis, respectively. In this study, we report a distinct metabolic circuit of catabolic metabolism in breast cancer subtypes. Interestingly, PFKP and FBP1 are inversely correlated in clinical samples, indicating different metabolic subsets of breast cancer. The luminal types of breast cancer consist of the pentose phosphate pathway (PPP) subset by suppression of PFKP while the basal-like subtype (also known as triple negative breast cancer, TNBC) mainly utilizes glycolysis and mitochondrial fatty acid oxidation (FAO) by loss of FBP1 and ACC2. Notably, PPP remains active via upregulation of TIGAR in the FBP1-loss basal-like subset, indicating the importance of PPP in catabolic cancer metabolism. These results indicate different catabolic metabolic circuits and thus therapeutic strategies in breast cancer subsets.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherMDPI-
dc.relation.isPartOfCELLS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.titleBreast Cancer Subtypes Underlying EMT-Mediated Catabolic Metabolism-
dc.typeArticle-
dc.contributor.collegeResearch Institutes (연구소)-
dc.contributor.departmentOral Cancer Research Institute (구강종양연구소)-
dc.contributor.googleauthorEunae Sandra Cho-
dc.contributor.googleauthorNam Hee Kim-
dc.contributor.googleauthorJun Seop Yun-
dc.contributor.googleauthorSue Bean Cho-
dc.contributor.googleauthorHyun Sil Kim-
dc.contributor.googleauthorJong In Yook-
dc.identifier.doi10.3390/cells9092064-
dc.contributor.localIdA00360-
dc.contributor.localIdA01121-
dc.contributor.localIdA01121-
dc.contributor.localIdA02536-
dc.contributor.localIdA02536-
dc.contributor.localIdA04799-
dc.contributor.localIdA04799-
dc.relation.journalcodeJ03774-
dc.identifier.pmid32927665-
dc.subject.keywordEMT-
dc.subject.keywordSnail-
dc.subject.keywordbreast cancer subtypes-
dc.subject.keywordcatabolic metabolism-
dc.contributor.alternativeNameKim, Nam Hee-
dc.contributor.affiliatedAuthor김남희-
dc.contributor.affiliatedAuthor김현실-
dc.contributor.affiliatedAuthor김현실-
dc.contributor.affiliatedAuthor육종인-
dc.contributor.affiliatedAuthor육종인-
dc.contributor.affiliatedAuthor조은애산드라-
dc.contributor.affiliatedAuthor조은애산드라-
dc.citation.volume9-
dc.citation.number9-
dc.citation.startPage2064-
dc.identifier.bibliographicCitationCELLS, Vol.9(9) : 2064, 2020-09-
Appears in Collections:
5. Research Institutes (연구소) > Oral Cancer Research Institute (구강종양연구소) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Oral Pathology (구강병리학교실) > 1. Journal Papers

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