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https://hdl.handle.net/11147/12414
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DC Field | Value | Language |
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dc.contributor.author | Uğur, Deniz | - |
dc.contributor.author | Güngül, Taha Buğra | - |
dc.contributor.author | Yücel, Simge | - |
dc.contributor.author | Özçivici, Engin | - |
dc.contributor.author | Yalçın Özuysal, Özden | - |
dc.contributor.author | Meşe Özçivici, Gülistan | - |
dc.date.accessioned | 2022-08-24T17:47:10Z | - |
dc.date.available | 2022-08-24T17:47:10Z | - |
dc.date.issued | 2022-07 | - |
dc.identifier.issn | 1873-9601 | - |
dc.identifier.uri | http://dx.doi.org/10.1007/s12079-021-00665-9 | - |
dc.identifier.uri | https://hdl.handle.net/11147/12414 | - |
dc.description.abstract | Connexins (Cx) are primary components of gap junctions that selectively allow molecules to be exchanged between adjacent cells, regulating multiple cellular functions. Along with their channel forming functions, connexins play a variety of roles in different stages of tumorigenesis and their roles in tumor initiation and progression is isoform- and tissue-specific. While Cx26 and Cx43 were downregulated during breast tumorigenesis, Cx32 was accumulated in the cytoplasm of the cells in lymph node metastasis of breast cancers and Cx32 was further upregulated in metastasis. Cx32's effect on cell proliferation, gap junctional communication, hemichannel activity, cellular motility and epithelial-to-mesenchymal transition (EMT) were investigated by overexpressing Cx32 in Hs578T and MCF7 breast cancer cells. Additionally, the expression and localization of Cx26 and Cx43 upon Cx32 overexpression were examined by Western blot and immunostaining experiments, respectively. We observed that MCF7 cells had endogenous Cx32 while Hs578T cells did not and when Cx32 was overexpressed in these cells, it caused a significant increase in the percentages of Hs578T cells at the S phase in addition to increasing their proliferation. Further, while Cx32 overexpression did not induce hemichannel activity in either cell, it decreased gap junctional communication between Hs578T cells. Additionally, Cx32 was mainly observed in the cytoplasm in both cells, where it did not form gap junction plaques but Cx32 overexpression reduced Cx43 levels without affecting Cx26. Moreover, migration and invasion potentials of Hs578T and migration in MCF7 were reduced upon Cx32 overexpression. Finally, the protein level of mesenchymal marker N-cadherin decreased while epithelial marker ZO-1 and E-cadherin increased in Hs578T cells. We observed that Cx32 overexpression altered cell proliferation, communication, migration and EMT in Hs578T, suggesting a tumor suppressor role in these cells while it had minor effects on MCF7 cells. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Springer | en_US |
dc.relation | Connexin 32’nin Farklı Metastatik Özellikleri Olan Meme Kanseri Hücrelerinde Oynadığı Rollerin Araştırılması | en_US |
dc.relation.ispartof | Journal of Cell Communication and Signaling | en_US |
dc.rights | info:eu-repo/semantics/embargoedAccess | en_US |
dc.subject | Connexin 32 | en_US |
dc.subject | Breast cancer | en_US |
dc.subject | Proliferation | en_US |
dc.title | Connexin 32 Overexpression Increases Proliferation, Reduces Gap Junctional Intercellular Communication, Motility and Epithelial-To Transition in Hs578t Breast Cancer Cells | en_US |
dc.type | Article | en_US |
dc.authorid | 0000-0002-5240-511X | - |
dc.authorid | 0000-0001-7632-4456 | - |
dc.authorid | 0000-0003-4464-0475 | - |
dc.authorid | 0000-0003-0552-368X | - |
dc.authorid | 0000-0003-0458-8684 | - |
dc.authorid | 0000-0002-5240-511X | - |
dc.authorid | 0000-0001-7632-4456 | - |
dc.authorid | 0000-0003-4464-0475 | - |
dc.authorid | 0000-0003-0552-368X | - |
dc.authorid | 0000-0003-0458-8684 | - |
dc.institutionauthor | Uğur, Deniz | - |
dc.institutionauthor | Güngül, Taha Buğra | - |
dc.institutionauthor | Yücel, Simge | - |
dc.institutionauthor | Özçivici, Engin | - |
dc.institutionauthor | Yalçın Özuysal, Özden | - |
dc.institutionauthor | Meşe Özçivici, Gülistan | - |
dc.department | İzmir Institute of Technology. Molecular Biology and Genetics | en_US |
dc.department | İzmir Institute of Technology. Bioengineering | en_US |
dc.identifier.wos | WOS:000820568100001 | - |
dc.identifier.scopus | 2-s2.0-85133353829 | - |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.identifier.doi | 10.1007/s12079-021-00665-9 | - |
dc.identifier.pmid | 35781670 | - |
dc.contributor.affiliation | 01. Izmir Institute of Technology | en_US |
dc.contributor.affiliation | 01. Izmir Institute of Technology | en_US |
dc.contributor.affiliation | 01. Izmir Institute of Technology | en_US |
dc.contributor.affiliation | 01. Izmir Institute of Technology | en_US |
dc.contributor.affiliation | 01. Izmir Institute of Technology | en_US |
dc.contributor.affiliation | 01. Izmir Institute of Technology | en_US |
dc.relation.issn | 1873-9601 | en_US |
dc.relation.grantno | 114Z874 | en_US |
dc.identifier.wosquality | Q3 | - |
dc.identifier.scopusquality | Q3 | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.languageiso639-1 | en | - |
item.openairetype | Article | - |
item.grantfulltext | embargo_20250701 | - |
item.fulltext | With Fulltext | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | 01. Izmir Institute of Technology | - |
crisitem.author.dept | 01. Izmir Institute of Technology | - |
crisitem.author.dept | 01. Izmir Institute of Technology | - |
crisitem.author.dept | 03.01. Department of Bioengineering | - |
crisitem.author.dept | 04.03. Department of Molecular Biology and Genetics | - |
crisitem.author.dept | 04.03. 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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File | Description | Size | Format | |
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s12079-021-00665-9.pdf Until 2025-07-01 | Article | 5.96 MB | Adobe PDF | View/Open |
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