Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/46730
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dc.contributor.authorEngur-Ozturk, Selin-
dc.contributor.authorDikmen, Miris-
dc.date.accessioned2023-01-09T21:15:54Z-
dc.date.available2023-01-09T21:15:54Z-
dc.date.issued2022-
dc.identifier.issn0301-4851-
dc.identifier.issn1573-4978-
dc.identifier.urihttps://doi.org/10.1007/s11033-022-07329-w-
dc.identifier.urihttps://hdl.handle.net/11499/46730-
dc.description.abstractBackground Lung cancer is a leading cause of cancer-related deaths, primarily as a result of metastases. In this metastasis, the epithelial-to-mesenchymal transition (EMT) is essential. Interaction with the cancer cell microenvironment is primarily dependent on M1- and M2-polarized macrophage. Methods and results In this study, we revealed the EMT-associated activity of M1, M2a and M2c macrophages in A549 lung cancer cells. We established a co-culture model of A549 lung cancer cells utilizing THP-1-derived M1/M2 polarised macrophages to explore the involvement of macrophages in the immune response, apoptosis, and EMT in lung cancer. Although multiple polarising agents are routinely used for M1 and M2 conversion, we assessed a new possible polarising agent, hydrocortisone. Conclusions M1 increased A549 cell sensitivity to proteasome inhibitors and decreased A549 cell viability by inducing apoptosis. EMT was induced in the presence of M2c macrophages in A549 cells by the levels of vimentin, fibronectin, E-cadherin, NF-kB, CCL-17. We also revealed the antiproliferative effects of bortezomib and ixazomib on A549 cells in both 2D and 3D cultures. Our findings could help develop an immunotherapeutic strategy by shedding light on a previously undiscovered part of the EMT pathway. Furthermore, additional investigation may reveal that polarising tumour-associated macrophages to M1 and eliminating the M2a or particularly the M2c subtype are effective anti-cancer strategies.en_US
dc.description.sponsorshipAnadolu University Scientific Research Projects [1704S095]en_US
dc.description.sponsorshipThis study was funded by Anadolu University Scientific Research Projects (grant number 1704S095.).en_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofMolecular Biology Reportsen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectA549en_US
dc.subjectMacrophagesen_US
dc.subjectEMTen_US
dc.subjectNF-kBen_US
dc.subjectBortezomiben_US
dc.subjectIxazomiben_US
dc.subjectAlternative Activationen_US
dc.subjectTumor-Growthen_US
dc.subjectKappa-Ben_US
dc.subjectMetastasisen_US
dc.subjectMln2238en_US
dc.subjectMarkeren_US
dc.subjectEmten_US
dc.titleProteasome inhibitor immunotherapy for the epithelial to mesenchymal transition: assessing the A549 lung cancer cell microenvironment and the role of M1, M2a and M2c 'hydrocortisone-polarised' macrophagesen_US
dc.typeArticleen_US
dc.identifier.volume49en_US
dc.identifier.issue6en_US
dc.identifier.startpage4777en_US
dc.identifier.endpage4793en_US
dc.authoridEngur Ozturk, Selin/0000-0003-1534-8117-
dc.identifier.doi10.1007/s11033-022-07329-w-
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.authorscopusid57226403029-
dc.authorscopusid14026554000-
dc.identifier.pmid35279785en_US
dc.identifier.scopus2-s2.0-85126148913en_US
dc.identifier.wosWOS:000768120100001en_US
local.message.claim2023-07-10T21:26:44.214+0300|||rp01402|||submit_approve|||dc_contributor_author|||None*
dc.identifier.scopusqualityQ2-
item.grantfulltextopen-
item.fulltextWith Fulltext-
item.cerifentitytypePublications-
item.openairetypeArticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
crisitem.author.dept37.01. Pharmacy Services-
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tavas Sağlık Hizmetleri Meslek Yüksekokulu Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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