Publication:
Targeting the epithelial-mesenchymal transition (emt) pathway with combination of wnt inhibitor and chalcone complexes in lung cancer cells

dc.contributor.authorCoşkun, Demet
dc.contributor.buuauthorArı, Ferda
dc.contributor.buuauthorARI, FERDA
dc.contributor.buuauthorErtürk, Elif
dc.contributor.buuauthorERTÜRK, ELİF
dc.contributor.buuauthorOnur, Ömer E.
dc.contributor.buuauthorAkgün, Oğuzhan
dc.contributor.buuauthorAydın, İpek
dc.contributor.buuauthorİPEK, AYDIN
dc.contributor.departmentBursa Uludağ Üniversitesi/Fen Edebiyat Fakültesi/Biyoloji Bölümü.
dc.contributor.departmentBursa Uludağ Üniversitesi/Tıbbi Labaratuvar Teknikleri .
dc.contributor.orcid0000-0002-8410-1786
dc.contributor.orcid0000-0002-6729-7908
dc.contributor.researcheridA-5608-2019
dc.contributor.researcheridJQI-3400-2023
dc.contributor.researcheridAAG-7012-2021
dc.contributor.researcheridIUO-8513-2023
dc.date.accessioned2024-11-01T05:42:04Z
dc.date.available2024-11-01T05:42:04Z
dc.date.issued2023-07-14
dc.description.abstractNon-small cell lung cancer (NSCLC) is the most common type of the lung cancer. Despite development in treatment options in NSCLC, the overall survival ratios is still poor due to epithelial and mesenchymal transition (EMT) feature and associated metastasis event. Thereby there is a need to develop strategy to increase antitumor response against the NSCLC cells by targeting EMT pathway with combination drugs. Niclosamide and chalcone complexes are both affect cancer cell signaling pathways and therefore inhibit the EMT pathway. In this study, it was aimed to increase antitumor response and suppress EMT pathway in NSCLC cells by combining niclosamide and chalcone complexes. SRB cell viability assay was performed to investigate the anticancer activity of drugs. The drugs were tested on both NSCLC cells (A549 and H1299) and normal lung bronchial cells (BEAS-2B). Then the two drugs were combined and their effects on cancer cells were evaluated. Fluorescence imaging and enzyme-linked immunosorbent assay were performed on treated cells to observe the cell death manner. Wound healing assay, real-time quantitative polymerase chain reaction, and western blot analysis were performed to measure EMT pathway activity. Our results showed that niclosamide and chalcone complexes combination kill cancer cells more than normal lung bronchial cells. Compared to single drug administration, the combination of both drugs killed NSCLC cells more effectively by increasing apoptotic activity. In addition, the combination of niclosamide and chalcone complexes decreased multidrug resistance and EMT activity by lowering their gene expressions and protein levels. These results showed that niclosamide and chalcone complexes combination could be a new drug combination for the treatment of NSCLC.
dc.description.sponsorshipCouncil of Higher Education FGA-2021-374
dc.description.sponsorshipCouncil of Higher Education (YOEK) 100/2000 PhD Scholarship Program
dc.identifier.doi10.1002/jcb.30442
dc.identifier.endpage1219
dc.identifier.issn0730-2312
dc.identifier.issue8
dc.identifier.startpage1203
dc.identifier.urihttps://doi.org/10.1002/jcb.30442
dc.identifier.urihttps://hdl.handle.net/11452/47288
dc.identifier.volume124
dc.identifier.wos001028035800001
dc.indexed.wosWOS.SCI
dc.language.isoen
dc.publisherWiley
dc.relation.bapBAP
dc.relation.journalJournal Of Cellular Biochemistry
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectExperimental-design
dc.subjectIn-vitro
dc.subjectNiclosamide
dc.subjectResistance
dc.subjectApoptosis
dc.subjectSnail
dc.subjectChalcone complexes
dc.subjectDrug resistance
dc.subjectEpithelial-mesenchymal transition (emt)
dc.subjectNsclc
dc.subjectScience & technology
dc.subjectLife sciences & biomedicine
dc.subjectBiochemistry & molecular biology
dc.subjectBiochemistry & molecular biology
dc.subjectCell biology
dc.titleTargeting the epithelial-mesenchymal transition (emt) pathway with combination of wnt inhibitor and chalcone complexes in lung cancer cells
dc.typeArticle
dspace.entity.typePublication
relation.isAuthorOfPublication1dd517bb-3e11-411e-a8db-27d448dcd55e
relation.isAuthorOfPublication54fbb8ee-6806-4d77-9430-9b360d81a2ab
relation.isAuthorOfPublication5a1dd361-f549-401f-9131-862a6347b97f
relation.isAuthorOfPublication.latestForDiscovery1dd517bb-3e11-411e-a8db-27d448dcd55e

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