Naringin Combined with NF-?B Inhibition and Endoplasmic Reticulum Stress Induces Apoptotic Cell Death via Oxidative Stress and the PERK/eIF2?/ATF4/CHOP Axis in HT29 Colon Cancer Cells

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dc.authoridDoganlar, Zeynep Banu/0000-0002-1365-9897
dc.authoridDOĞAN, AYTEN/0000-0003-2525-785X
dc.authoridTurker, Nebiye Pelin/0000-0001-6060-3557
dc.authorwosidDoganlar, Zeynep Banu/B-4845-2008
dc.authorwosidDoğanlar, Oğuzhan/A-2315-2019
dc.authorwosidDOĞAN, AYTEN/ABA-6754-2020
dc.authorwosidTurker, Nebiye Pelin/AAH-3197-2021
dc.contributor.authorAlbayrak, Dogan
dc.contributor.authorDoganlar, Oguzhan
dc.contributor.authorErdogan, Suat
dc.contributor.authorMerakli, Meryem
dc.contributor.authorDogan, Ayten
dc.contributor.authorTurker, Pelin
dc.contributor.authorBostanci, Ayten
dc.date.accessioned2024-06-12T11:08:59Z
dc.date.available2024-06-12T11:08:59Z
dc.date.issued2021
dc.departmentTrakya Üniversitesien_US
dc.description.abstractCurrently, combination therapy is considered the most effective solution for a selective chemotherapeutic effect in the treatment of colon cancer. This study investigated the death of both colon cancer HT29 cells and healthy vascular smooth muscle TG-Ha-VSMC cells (VSMCs) induced by naringin combined with endoplasmic reticulum (ER) stress and NF-kappa B inhibition. Naringin combined with tunicamycin and BAY 11-7082 suppressed the proliferation of HT29 cells in a dose-dependent manner and induced particularly apoptotic death without significantly affecting healthy VSMCs according to Annexin V/PI staining and AO/EB staining analyses. Insufficient antioxidant defense and heat shock response as well as excessive ROS generation were observed in HT29 cells following combination therapy. Quantitative real-time PCR and western blot analysis demonstrated that drug combination-induced mitochondrial apoptosis was activated through the ROS-mediated PERK/eIF2 alpha/ATF4/CHOP pathway. Additionally, naringin combination significantly reduced the sXBP expression induced by tunicamycin+BAY 11-7082 in a dose-dependent manner. In conclusion, this study found that naringin combined with tunicamycin+BAY 11-7082 efficiently induced apoptotic cell death in HT29 colon cancer cells via oxidative stress and the PERK/eIF2 alpha/ATF4/CHOP pathway, suggesting that naringin combined with tunicamycin plus BAY 11-7082 could be a new combination therapy strategy for effective colon cancer treatment with minimal side effects on healthy cells.en_US
dc.description.sponsorshipTrakya University Scientific Research Fund [TUBAP 2016/42]en_US
dc.description.sponsorshipThis study was supported by the Trakya University Scientific Research Fund (TUBAP 2016/42).en_US
dc.identifier.doi10.1007/s10528-020-09996-5
dc.identifier.endpage184en_US
dc.identifier.issn0006-2928
dc.identifier.issn1573-4927
dc.identifier.issue1en_US
dc.identifier.pmid32979141en_US
dc.identifier.scopus2-s2.0-85091422998en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage159en_US
dc.identifier.urihttps://doi.org/10.1007/s10528-020-09996-5
dc.identifier.urihttps://hdl.handle.net/20.500.14551/22646
dc.identifier.volume59en_US
dc.identifier.wosWOS:000572866500001en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringer/Plenum Publishersen_US
dc.relation.ispartofBiochemical Geneticsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectNaringinen_US
dc.subjectTunicamycinen_US
dc.subjectBAY 11-7082en_US
dc.subjectER Stressen_US
dc.subjectApoptosisen_US
dc.subjectColon Canceren_US
dc.subjectUnfolded Protein Responseen_US
dc.subjectEr Stressen_US
dc.subjectMitochondrial Apoptosisen_US
dc.subjectSignaling Pathwayen_US
dc.subjectLeukemia-Cellsen_US
dc.subjectActivationen_US
dc.subjectCarcinomaen_US
dc.subjectGrowthen_US
dc.subjectExpressionen_US
dc.subjectArresten_US
dc.titleNaringin Combined with NF-?B Inhibition and Endoplasmic Reticulum Stress Induces Apoptotic Cell Death via Oxidative Stress and the PERK/eIF2?/ATF4/CHOP Axis in HT29 Colon Cancer Cellsen_US
dc.typeArticleen_US

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