Systematic identification of a nuclear receptor-enriched predictive signature for erastin-induced ferroptosis

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dc.contributor.authorOk Seon Kwon-
dc.contributor.authorE J Kwon-
dc.contributor.authorH J Kong-
dc.contributor.authorJ Y Choi-
dc.contributor.authorY J Kim-
dc.contributor.authorEun-Woo Lee-
dc.contributor.authorW Kim-
dc.contributor.authorH Lee-
dc.contributor.authorH J Cha-
dc.date.accessioned2020-10-04T13:15:31Z-
dc.date.available2020-10-04T13:15:31Z-
dc.date.issued2020-
dc.identifier.issn2213-2317-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/22910-
dc.description.abstractErastin, a synthetic lethal compound against cancer expressing an oncogenic RAS, inhibits cystine/glutamate antiporters and causes ferroptosis. However, despite recent evidence for the mechanisms underlying ferroptosis, molecular biomarkers of erastin-dependent ferroptosis have not been identified. Here, we employed isogenic lung cancer cell models to show that a redox imbalance leads to glutathione depletion and ferroptosis. Subsequent transcriptome analysis of pan-cancer cell lines revealed that the activity of transcription factors, including NRF2 and AhR, serve as important markers of erastin resistance. Based on the integrated expression of genes in the nuclear receptor meta-pathway (NRM), we constructed an NRM model and validated its robustness using an independent pharmacogenomics dataset. The NRM model was further evaluated by sensitivity tests on nine cancer cell lines for which erastin sensitivities had not been determined. Our pharmacogenomics approach has the potential to pave the way for the efficient classification of patients for therapeutic intervention using erastin.-
dc.publisherElsevier-
dc.titleSystematic identification of a nuclear receptor-enriched predictive signature for erastin-induced ferroptosis-
dc.title.alternativeSystematic identification of a nuclear receptor-enriched predictive signature for erastin-induced ferroptosis-
dc.typeArticle-
dc.citation.titleRedox Biology-
dc.citation.number0-
dc.citation.endPage101719-
dc.citation.startPage101719-
dc.citation.volume37-
dc.contributor.affiliatedAuthorOk Seon Kwon-
dc.contributor.affiliatedAuthorEun-Woo Lee-
dc.contributor.alternativeName권옥선-
dc.contributor.alternativeName권은지-
dc.contributor.alternativeName공현준-
dc.contributor.alternativeName최정윤-
dc.contributor.alternativeName김윤정-
dc.contributor.alternativeName이은우-
dc.contributor.alternativeName김완규-
dc.contributor.alternativeName이해승-
dc.contributor.alternativeName차혁진-
dc.identifier.bibliographicCitationRedox Biology, vol. 37, pp. 101719-101719-
dc.identifier.doi10.1016/j.redox.2020.101719-
dc.subject.keywordErastin-
dc.subject.keywordFerroptosis-
dc.subject.keywordRedox imbalance-
dc.subject.keywordNRF2-
dc.subject.keywordAryl hydrocarbon receptor-
dc.subject.keywordElastic net-
dc.subject.keywordDrug response biomarker-
dc.subject.keywordDrug sensitivity prediction-
dc.subject.localerastin-
dc.subject.localErastin-
dc.subject.localferroptosis-
dc.subject.localFerroptosis-
dc.subject.localRedox imbalance-
dc.subject.localNRF2-
dc.subject.localNrf2-
dc.subject.localNrf-2-
dc.subject.localAryl hydrocarbon receptor-
dc.subject.localElastic net-
dc.subject.localDrug response biomarker-
dc.subject.localDrug sensitivity prediction-
dc.description.journalClassY-
Appears in Collections:
Division of Research on National Challenges > Stem Cell Convergenece Research Center > 1. Journal Articles
Division of Biomedical Research > Metabolic Regulation Research Center > 1. Journal Articles
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