Cited 16 times in

Nicotinamide (niacin) supplement increases lipid metabolism and ROS-induced energy disruption in triple-negative breast cancer: potential for drug repositioning as an anti-tumor agent

DC Field Value Language
dc.contributor.author정민선-
dc.date.accessioned2022-07-08T03:07:46Z-
dc.date.available2022-07-08T03:07:46Z-
dc.date.issued2022-05-
dc.identifier.issn1574-7891-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/188679-
dc.description.abstractMetabolic dysregulation is an important hallmark of cancer. Nicotinamide (NAM), a water-soluble amide form of niacin (vitamin B3), is currently available as a supplement for maintaining general physiologic functions. NAM is a crucial regulator of mitochondrial metabolism and redox reactions. In this study, we aimed to identify the mechanistic link between NAM-induced metabolic regulation and the therapeutic efficacy of NAM in triple-negative breast cancer (TNBC). The combined analysis using multiomics systems biology showed that NAM decreased mitochondrial membrane potential and ATP production, but increased the activities of reverse electron transport (RET), fatty acid β-oxidation and glycerophospholipid/sphingolipid metabolic pathways in TNBC, collectively leading to an increase in the levels of reactive oxygen species (ROS). The increased ROS levels triggered apoptosis and suppressed tumour growth and metastasis of TNBC in both human organoids and xenograft mouse models. Our results showed that NAM treatment leads to cancer cell death in TNBC via mitochondrial dysfunction and activation of ROS by bifurcating metabolic pathways (RET and lipid metabolism); this provides insights into the repositioning of NAM supplement as a next-generation anti-metabolic agent for TNBC treatment.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherJohn Wiley & Sons, Inc-
dc.relation.isPartOfMOLECULAR ONCOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.subject.MESHAnimals-
dc.subject.MESHApoptosis-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHDrug Repositioning-
dc.subject.MESHHumans-
dc.subject.MESHLipid Metabolism-
dc.subject.MESHMice-
dc.subject.MESHNiacin* / pharmacology-
dc.subject.MESHNiacin* / therapeutic use-
dc.subject.MESHNiacinamide / pharmacology-
dc.subject.MESHNiacinamide / therapeutic use-
dc.subject.MESHReactive Oxygen Species / metabolism-
dc.subject.MESHTriple Negative Breast Neoplasms* / pathology-
dc.titleNicotinamide (niacin) supplement increases lipid metabolism and ROS-induced energy disruption in triple-negative breast cancer: potential for drug repositioning as an anti-tumor agent-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pathology (병리학교실)-
dc.contributor.googleauthorMinsun Jung-
dc.contributor.googleauthorKyung-Min Lee-
dc.contributor.googleauthorYebin Im-
dc.contributor.googleauthorSeung Hyeok Seok-
dc.contributor.googleauthorHyewon Chung-
dc.contributor.googleauthorDa Young Kim-
dc.contributor.googleauthorDohyun Han-
dc.contributor.googleauthorCheng Hyun Lee-
dc.contributor.googleauthorEun Hye Hwang-
dc.contributor.googleauthorSoo Young Park-
dc.contributor.googleauthorJiwon Koh-
dc.contributor.googleauthorBohyun Kim-
dc.contributor.googleauthorIlias P Nikas-
dc.contributor.googleauthorHyebin Lee-
dc.contributor.googleauthorDaehee Hwang-
dc.contributor.googleauthorHan Suk Ryu-
dc.identifier.doi10.1002/1878-0261.13209-
dc.contributor.localIdA06280-
dc.relation.journalcodeJ03480-
dc.identifier.eissn1878-0261-
dc.identifier.pmid35278276-
dc.subject.keywordmetabolism-
dc.subject.keywordnicotinamide-
dc.subject.keywordorganoids-
dc.subject.keywordproteogenomics-
dc.subject.keywordreactive oxygen species-
dc.subject.keywordtriple negative breast neoplasms.-
dc.contributor.alternativeNameJung, Minsun-
dc.contributor.affiliatedAuthor정민선-
dc.citation.volume16-
dc.citation.number9-
dc.citation.startPage1795-
dc.citation.endPage1815-
dc.identifier.bibliographicCitationMOLECULAR ONCOLOGY, Vol.16(9) : 1795-1815, 2022-05-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers

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