Curcumin activates ROS signaling to promote pyroptosis in hepatocellular carcinoma HepG2 cells

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dc.contributor.authorW F Liang-
dc.contributor.authorY X Gong-
dc.contributor.authorH F Li-
dc.contributor.authorF L Sun-
dc.contributor.authorW L Li-
dc.contributor.authorD Q Chen-
dc.contributor.authorD P Xie-
dc.contributor.authorC X Ren-
dc.contributor.authorX Y Guo-
dc.contributor.authorZ Y Wang-
dc.contributor.authorTaeho Kwon-
dc.contributor.authorH N Sun-
dc.date.accessioned2021-01-08T03:30:28Z-
dc.date.available2021-01-08T03:30:28Z-
dc.date.issued2021-
dc.identifier.issn0258-851X-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/23981-
dc.description.abstractBackground/aim: Curcumin is a polyphenol that exerts a variety of pharmacological activities and plays an anti-cancer role in many cancer cells. It was recently reported that gasdermin E (GSDME) is involved in the progression of pyroptosis. Materials and methods: HepG2 cells were treated with various concentrations of curcumin and cell viability was examined using MTT assay, apoptosis was analysed using flow cytometry, reactive oxygen species (ROS) levels using dihydroethidium, LDH release using an LDH cytotoxicity assay, and protein expression using western blot. Results: Curcumin increased the expression of the GSDME N-terminus and proteins involved in pyrolysis, promoted HspG2 cell pyrolysis and increased intracellular ROS levels. Moreover, inhibition of the production of intracellular ROS with n-acetylcysteine (NAC) improved the degree of apoptosis and pyrolysis induced by curcumin. Conclusion: Curcumin induces HspG2 cell death by increasing apoptosis and pyroptosis, and ROS play a key role in this process. This study improves our understanding of the potential anti-cancer properties of curcumin in liver cancer.-
dc.publisherInt Inst Anticancer Research-
dc.titleCurcumin activates ROS signaling to promote pyroptosis in hepatocellular carcinoma HepG2 cells-
dc.title.alternativeCurcumin activates ROS signaling to promote pyroptosis in hepatocellular carcinoma HepG2 cells-
dc.typeArticle-
dc.citation.titlein Vivo-
dc.citation.number1-
dc.citation.endPage257-
dc.citation.startPage249-
dc.citation.volume35-
dc.contributor.affiliatedAuthorTaeho Kwon-
dc.contributor.alternativeNameLiang-
dc.contributor.alternativeNameGong-
dc.contributor.alternativeNameLi-
dc.contributor.alternativeNameSun-
dc.contributor.alternativeNameLi-
dc.contributor.alternativeNameChen-
dc.contributor.alternativeNameXie-
dc.contributor.alternativeNameRen-
dc.contributor.alternativeNameGuo-
dc.contributor.alternativeNameWang-
dc.contributor.alternativeName권태호-
dc.contributor.alternativeNameSun-
dc.identifier.bibliographicCitationin Vivo, vol. 35, no. 1, pp. 249-257-
dc.identifier.doi10.21873/invivo.12253-
dc.subject.keywordCurcumin-
dc.subject.keywordGSDME-
dc.subject.keywordLiver cancer-
dc.subject.keywordProptosis-
dc.subject.keywordROS-
dc.subject.localCurcumin-
dc.subject.localcurcumin-
dc.subject.localGSDME-
dc.subject.localLiver cancer-
dc.subject.localliver cancer-
dc.subject.localLiver Cancer-
dc.subject.localProptosis-
dc.subject.localReactive oxidative species-
dc.subject.localReactive oxygen species(ROS)-
dc.subject.localReactive oxygen species-
dc.subject.localReactive Oxygen Species (ROS)-
dc.subject.localReactive Oxygen Species-
dc.subject.localROS-
dc.subject.localReactive oxygen species (ROS)-
dc.subject.localreactive oxygen species-
dc.subject.localreactive oxygen species (ROS)-
dc.description.journalClassY-
Appears in Collections:
Jeonbuk Branch Institute > Primate Resources Center > 1. Journal Articles
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