Please use this identifier to cite or link to this item: https://hdl.handle.net/11147/10382
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dc.contributor.authorAdak, Aslıtr
dc.contributor.authorÜnal, Yağmur Cerentr
dc.contributor.authorYücel, Simgetr
dc.contributor.authorVural, Zehratr
dc.contributor.authorTuran, Fatma Başaktr
dc.contributor.authorYalçın Özuysal, Özden-
dc.contributor.authorMeşe, Gülistantr
dc.date.accessioned2021-01-24T18:34:24Z-
dc.date.available2021-01-24T18:34:24Z-
dc.date.issued2020-
dc.identifier.issn0167-4889-
dc.identifier.issn1879-2596-
dc.identifier.urihttps://doi.org/10.1016/j.bbamcr.2020.118851-
dc.identifier.urihttps://hdl.handle.net/10382-
dc.description.abstractConnexins (Cx), the basic subunit of gap junctions, play important roles in cell homeostasis, and their abnormal expression and function are associated with human hereditary diseases and cancers. In tumorigenesis, connexins were observed to have both anti-tumorigenic and pro-tumorigenic roles in a context- and stage-dependent manner. Initially, Cx26 and Cx43 were thought to be the only connexins involved in normal breast homeostasis and breast cancer. Later on, association of Cx32 expression with lymph node metastasis of breast cancer and subsequent demonstration of its expression in normal breast tissue suggested that Cx32 contributes to breast tissue homeostasis. Here, we aimed to determine the effects of Cx32 on normal breast cells, MCF10A, and on breast cancer cells, MDA-MB-231. Cx32 overexpression had profound effects on MCF10A cells, decreasing cell proliferation by increasing the doubling time of MCF10A. Furthermore, MCF10A cells acquired mesenchymal-like appearance upon Cx32 expression and had increased migration capacity and expression of both E-cadherin and vimentin. In contrast, Cx32 overexpression altered the EMT markers of MDA-MB-231 by increasing the expression of mesenchymal markers, such as slug and vimentin, and decreasing E-cadherin expression without affecting their proliferation and morphology. Our results indicate, for the first time in the literature, that Cx32 has tumor-promoting roles in MCF10A and MDA-MB-231 cells.en_US
dc.description.sponsorshipWe thank Dr. Steven Scherer from University of Pennsylvania, PA, USA for kindly providing the pIRES2-EGFP2-Cx32 vector. Main financial support by The Scientific and Technological Research Council of Turkey (Grant number 114Z874 to GM) is gratefully acknowledged. The Young Investigator Award by the Turkish Academy of Sciences to GM is also highly appreciated. We also would like to thank the Biotechnology and Bioengineering Research and Application Center, Izmir Institute of Technology staff for their expert technical help. Finally, proofreading by the Academic Writing Center, Izmir Institute of Technology was greatly appreciated.en_US
dc.language.isoenen_US
dc.publisherElsevieren_US
dc.relation.ispartofBiochimica et Biophysica Acta - Molecular Cell Researchen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectConnexin 32en_US
dc.subjectProliferationen_US
dc.subjectMorphologyen_US
dc.subjectEMTen_US
dc.subjectBreast canceren_US
dc.titleConnexin 32 induces pro-tumorigenic features in MCF10A normal breast cells and MDA-MB-231 metastatic breast cancer cellsen_US
dc.typeArticleen_US
dc.institutionauthorAdak, Aslı-
dc.institutionauthorÜnal, Yağmur Ceren-
dc.institutionauthorYücel, Simge-
dc.institutionauthorVural, Zehra-
dc.institutionauthorTuran, Fatma Başak-
dc.institutionauthorYalçın Özuysal, Özden-
dc.departmentİzmir Institute of Technology. Molecular Biology and Geneticsen_US
dc.departmentİzmir Institute of Technology. Bioengineeringen_US
dc.identifier.volume1867en_US
dc.identifier.issue12en_US
dc.identifier.wosWOS:000576137700016en_US
dc.identifier.scopus2-s2.0-85091070097en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıtr
dc.identifier.doi10.1016/j.bbamcr.2020.118851-
dc.identifier.pmid32918981en_US
dc.relation.doi10.1016/j.bbamcr.2020.118851en_US
dc.coverage.doi10.1016/j.bbamcr.2020.118851en_US
dc.identifier.wosqualityQ2-
dc.identifier.scopusqualityQ2-
item.languageiso639-1en-
item.grantfulltextopen-
item.fulltextWith Fulltext-
item.cerifentitytypePublications-
item.openairetypeArticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.dept01. Izmir Institute of Technology-
crisitem.author.dept01. Izmir Institute of Technology-
crisitem.author.dept04.03. Department of Molecular Biology and Genetics-
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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