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HS-173 as a novel inducer of RIP3-dependent necroptosis in lung cancer

DC Field Value Language
dc.contributor.authorPark, JH-
dc.contributor.authorJung, KH-
dc.contributor.authorKim, SJ-
dc.contributor.authorYoon, YC-
dc.contributor.authorYan, HH-
dc.contributor.authorFang, Z-
dc.contributor.authorLee, JE-
dc.contributor.authorLim, JH-
dc.contributor.authorMah, S-
dc.contributor.authorHong, S-
dc.contributor.authorKim, YS-
dc.contributor.authorHong, SS-
dc.date.accessioned2020-11-17T05:25:19Z-
dc.date.available2020-11-17T05:25:19Z-
dc.date.issued2019-
dc.identifier.issn0304-3835-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/19054-
dc.description.abstractNecroptosis is a form of regulated necrotic cell death mediated by receptor-interacting kinase 3 (RIP3). Recently, necroptosis has gained attention as a novel alternative therapy to target cancer cells. In this study, we screened several chemotherapeutics used in preclinical and clinical studies, and identified a drug HS-173 that induces RIP3-mediated necroptosis. HS-173 decreased the cell survival in a dose-dependent manner in RIP3-expressing lung cancer cells, compared to the cells lacking RIP3. Also, the cell death induced by HS-173 was rescued by specific necroptosis inhibitors such as necrostatin-1 and dabrafenib. Additionally, HS-173 increased the phosphorylation of RIP3 and MLKL, which was decreased by necroptosis inhibitors, indicating that HS-173 activates RIP3/MLKL signaling in lung cancer cells. HS-173 increased the necroptotic events, as observed by the increased levels of HMGB1 and necroptotic morphological features. Furthermore, HS-173 inhibited the tumor growth by stimulation of necroptosis in mouse xenograft models. Our findings offer new insights into the role of HS-173 in inducing necroptosis by enhancing RIP3 expression and activating the RIP3/MLKL signaling pathway in lung cancer cells.-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHApoptosis-
dc.subject.MESHCell Proliferation-
dc.subject.MESHGene Expression Regulation, Neoplastic-
dc.subject.MESHHumans-
dc.subject.MESHLung Neoplasms-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred BALB C-
dc.subject.MESHMice, Nude-
dc.subject.MESHNecrosis-
dc.subject.MESHPhosphorylation-
dc.subject.MESHPyridines-
dc.subject.MESHReactive Oxygen Species-
dc.subject.MESHReceptor-Interacting Protein Serine-Threonine Kinases-
dc.subject.MESHSignal Transduction-
dc.subject.MESHSulfonamides-
dc.subject.MESHTumor Cells, Cultured-
dc.subject.MESHXenograft Model Antitumor Assays-
dc.titleHS-173 as a novel inducer of RIP3-dependent necroptosis in lung cancer-
dc.typeArticle-
dc.identifier.pmid30583075-
dc.subject.keywordHS-173-
dc.subject.keywordLung cancer-
dc.subject.keywordMLKL-
dc.subject.keywordNecroptosis-
dc.subject.keywordRIP3-
dc.contributor.affiliatedAuthor김, 유선-
dc.type.localJournal Papers-
dc.identifier.doi10.1016/j.canlet.2018.12.006-
dc.citation.titleCancer letters-
dc.citation.volume444-
dc.citation.date2019-
dc.citation.startPage94-
dc.citation.endPage104-
dc.identifier.bibliographicCitationCancer letters, 444. : 94-104, 2019-
dc.embargo.liftdate9999-12-31-
dc.embargo.terms9999-12-31-
dc.identifier.eissn1872-7980-
dc.relation.journalidJ003043835-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
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