Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/12287
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dc.contributor.authorGünyüz, Zehra Elifen_US
dc.contributor.authorSahi İlhan, Eceen_US
dc.contributor.authorKüçükköse, Cansuen_US
dc.contributor.authorİpekgil, Doğaçen_US
dc.contributor.authorTok, Güneşen_US
dc.contributor.authorMeşe, Gülistanen_US
dc.contributor.authorÖzçivici, Enginen_US
dc.contributor.authorYalçın Özuysal, Özdenen_US
dc.date.accessioned2022-08-09T13:58:45Z-
dc.date.available2022-08-09T13:58:45Z-
dc.date.issued2022-
dc.identifier.urihttps://doi.org/10.1021/acsomega.2c00840-
dc.identifier.urihttps://hdl.handle.net/11147/12287-
dc.description.abstractSemaphorin 6D (SEMA6D), a member of the class 6 semaphorin family, is a membrane-associated protein that plays a key role in the development of cardiac and neural tissues. A growing body of evidence suggests that SEMA6D is also involved in tumorigenesis. In breast cancer, high SEMA6D levels are correlated with better survival rates. However, very little is known about the functional significance of SEMA6D in breast tumorigenesis. In the present study, we aimed to investigate the effects of SEMA6D expression on the normal breast cell line MCF10A and the breast cancer cell lines MCF7 and MDA MB 231. We demonstrated that SEMA6D expression increases the proliferation of MCF10A cells, whereas the opposite effect was observed in MCF7 cells. SEMA6D expression induced anchorage-independent growth in both cancer cell lines. Furthermore, migration of MCF10A and MCF7 cells and invasion of MDA MB 231 cells were elevated in response to SEMA6D overexpression. Accordingly, the genes related to epithelial-mesenchymal transition (EMT) were altered by SEMA6D expression in MCF10A and MCF7 cell lines. Finally, we provided evidence that SEMA6D levels were associated with the expression of the cell cycle, EMT, and Notch signaling pathway-related genes in breast cancer patients' data. We showed for the first time that SEMA6D overexpression has cell-specific effects on the proliferation, migration, and invasion of normal and cancer breast cell lines, which agrees with the gene expression data of clinical samples. This study lays the groundwork for future research into understanding the functional importance of SEMA6D in breast canceren_US
dc.language.isoenen_US
dc.publisherAmerican Chemical Societyen_US
dc.relationMeme kanseri hücre hatlarında SEMA6D lokalizasyonunun belirlenmesien_US
dc.relation.ispartofACS Omegaen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectSEMA6Den_US
dc.subjectBreast canceren_US
dc.subjectBreast cellsen_US
dc.subjectCancer cell linesen_US
dc.titleSEMA6D differentially regulates proliferation, migration, and invasion of breast cell linesen_US
dc.typeArticleen_US
dc.authorid0000-0003-0458-8684en_US
dc.authorid0000-0003-4464-0475en_US
dc.authorid0000-0003-0552-368Xen_US
dc.departmentİzmir Institute of Technology. Molecular Biology and Geneticsen_US
dc.departmentİzmir Institute of Technology. Bioengineeringen_US
dc.identifier.wosWOS:000812823500001en_US
dc.identifier.scopus2-s2.0-85129344325en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.doi10.1021/acsomega.2c00840-
dc.identifier.pmid35571788-
dc.contributor.affiliation01. Izmir Institute of Technologyen_US
dc.contributor.affiliation01. Izmir Institute of Technologyen_US
dc.contributor.affiliation01. Izmir Institute of Technologyen_US
dc.contributor.affiliation01. Izmir Institute of Technologyen_US
dc.contributor.affiliation01. Izmir Institute of Technologyen_US
dc.contributor.affiliation01. Izmir Institute of Technologyen_US
dc.contributor.affiliation01. Izmir Institute of Technologyen_US
dc.contributor.affiliation01. Izmir Institute of Technologyen_US
dc.relation.issn2470-1343en_US
dc.relation.grantno2016IYTE65en_US
dc.identifier.scopusqualityQ1-
item.grantfulltextopen-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.openairetypeArticle-
item.languageiso639-1en-
item.fulltextWith Fulltext-
crisitem.author.dept04.03. Department of Molecular Biology and Genetics-
crisitem.author.dept03.01. Department of Bioengineering-
crisitem.author.dept04.03. Department of Molecular Biology and Genetics-
Appears in Collections:Bioengineering / Biyomühendislik
Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik
PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection
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