Cetuximab enhances oridonin-induced apoptosis through mitochondrial pathway and endoplasmic reticulum stress in laryngeal squamous cell carcinoma cells

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dc.contributor.authorDonkor, P.O.
dc.contributor.authorKang, N.
dc.contributor.authorCao, S.
dc.contributor.authorJiang, B.
dc.contributor.authorZhang, Q.
dc.contributor.authorZhu, Y.
dc.contributor.authorQiu, F.
dc.contributor.authorGao, X.
dc.date.accessioned2020-07-08T12:39:48Z
dc.date.available2020-07-08T12:39:48Z
dc.date.issued2020-05-12
dc.descriptionResearch Articleen_US
dc.description.abstractCetuximab plus oridonin showed a synergistic way to kill laryngeal squamous cell carcinoma (LSCC), as been reported previously. The present work further mechanistically extended action of the synergistic effects of combination treatment. Firstly, two LSCC cells displayed higher sensitivity to oridonin, whereas both low EGFR expression tumor cells and EGFR knockdown LSCC cells were less sensitive to oridonin. Next, cetuximab/oridonin significantly enhanced the mitochondrial apoptosis through NF-κB. Meanwhile, PI3K/Akt and JAK2/STAT3 pathways are associated with the nucleus translocation of NF-κB by combination treatment. Additionally, cetuximab enhanced oridonin-promoted ER stress-related apoptosis. Interestingly, both ER stress and mitochondrial apoptosis by combination treatment are abrogated by ROS scavenger. Furthermore, oridonin/cetuximab induced ROS production after 1.5 h, followed by G2/M arrest and apoptosis, indicating that ROS generation might be an early and key event. Taken together, cetuximab enhances oridonin-induced ER stress and mitochondrial apoptotic pathway, which contributes to the synergistic antitumor effects of cetuximab/oridonin.en_US
dc.description.sponsorshipNational Natural Science Foundation of China [grant numbers 81373797, 81102855]. the China Postdoctoral Science Special Foundation [grant number 2014T70224]; the China Postdoctoral Science Foundation [grant number 2013M541192].en_US
dc.identifier.otherhttps://doi.org/10.1016/j.tiv.2020.104885
dc.identifier.urihttp://ugspace.ug.edu.gh/handle/123456789/35491
dc.language.isoenen_US
dc.publisherToxicology in Vitroen_US
dc.relation.ispartofseries67;2020
dc.subjectCetuximaben_US
dc.subjectOridoninen_US
dc.subjectLaryngeal squamous cell carcinoma cellsen_US
dc.subjectSynergistic apoptosisen_US
dc.subjectER stressen_US
dc.subjectMitochondrial pathwayen_US
dc.titleCetuximab enhances oridonin-induced apoptosis through mitochondrial pathway and endoplasmic reticulum stress in laryngeal squamous cell carcinoma cellsen_US
dc.typeArticleen_US

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