Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/13980
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dc.contributor.authorSaydullaeva, Iroda-
dc.contributor.authorDebeleç Bütüner, Bilge-
dc.contributor.authorKorkmaz, Kemal Sami-
dc.date.accessioned2023-11-11T08:54:58Z-
dc.date.available2023-11-11T08:54:58Z-
dc.date.issued2023-
dc.identifier.issn2470-1343-
dc.identifier.urihttps://doi.org/10.1021/acsomega.3c03127-
dc.identifier.urihttps://hdl.handle.net/11147/13980-
dc.description.abstractStudies demonstrate that inflammation synergizes with highgrade aggressive prostate tumor development and ultimately metastatic spread, in which a lot of work has been done in recent years. However, the clear mechanism of inflammation inciting prostate cancer remains largely uncharacterized. Our previous study has shown that the conditioned media (CM)-mediated LNCaP cell migration is partially correlated with the loss of expression of the tumor suppressor NKX3.1. Here, we continue to investigate the inflammation-mediated migration of prostate cancer cells, and the role of NKX3.1 in this process to gain insights into cell migration-related changes comprehensively. Earlier, the model of inflammation in the tumor micro environment have been optimized by our research group; here, we continue to investigate the time-dependent effect of CM exposure together with NKX3.1 changes, in which we observed that these changes play important roles in gaining heterogeneous epithelial-to-mesenchymal transition (EMT) phenotype. Hence, this is an important parameter of tumor progression; we depleted NKX3.1 expression using the CRISPR/Cas9 system and examined the migrating cell clusters after exposure to inflammatory cytokines. We found that the migrated cells clearly demonstrate reversible loss of E-cadherin expression, which is consistent with subsequent vimentin expression alterations in comparison to control cells. Moreover, the data suggest that the AR mediated transcriptional program also contributes to mesenchymal-to-epithelial transition (MET) in prostate cancer progression. Furthermore, the quantitative proteomic analysis showed that migrated subpopulations from the same cell line presented different phenotypes in which the proteins overexpressed are involved in cell metabolism and RNA processing. According to KEGG pathway analysis, the ABC transporters were found to be the most significant. Thus, the dynamic process of cellular migration favors diverse genetic compositions under changing tumor microenvironments. The different levels of invasiveness are supported by shifting the cells in between these EMT and MET phenotypes.en_US
dc.description.sponsorshipThis research was supportedby TUBITAK 117S289 to K.S.K. Theauthors gratefully acknowledge the use of the services and facilitiesof the Koc University Proteomics Facility for proteomic analysis.The content is solely under the responsibility of the authors anddoes not necessarily represent the facility.en_US
dc.language.isoenen_US
dc.publisherAmerican Chemical Societyen_US
dc.relation.ispartofACS Omegaen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectInflammationen_US
dc.subjectMetastasisen_US
dc.subjectStatisticsen_US
dc.subjectOriginen_US
dc.titleNKX3.1 expression contributes to epithelial-mesenchymal transition of prostate cancer cellsen_US
dc.typeArticleen_US
dc.institutionauthorSaydullaeva, Iroda-
dc.departmentİzmir Institute of Technology. Rectorateen_US
dc.identifier.volume8en_US
dc.identifier.issue36en_US
dc.identifier.startpage32580en_US
dc.identifier.endpage32592en_US
dc.identifier.wosWOS:001061232300001en_US
dc.identifier.scopus2-s2.0-85172475581en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıtr
dc.identifier.doi10.1021/acsomega.3c03127-
dc.identifier.pmid37720744en_US
dc.identifier.scopusqualityQ1-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
item.languageiso639-1en-
item.openairetypeArticle-
item.cerifentitytypePublications-
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Rectorate / Rektörlük
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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