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https://hdl.handle.net/11499/10110
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DC Field | Value | Language |
---|---|---|
dc.contributor.author | Çetin, Gökhan Ozan | - |
dc.contributor.author | Toylu, Aslı | - |
dc.contributor.author | Atabey, Neşe | - |
dc.contributor.author | Sercan, Zeynep | - |
dc.contributor.author | Sakızlı, Meral | - |
dc.date.accessioned | 2019-08-16T13:11:38Z | |
dc.date.available | 2019-08-16T13:11:38Z | |
dc.date.issued | 2015 | - |
dc.identifier.issn | 1945-0265 | - |
dc.identifier.uri | https://hdl.handle.net/11499/10110 | - |
dc.identifier.uri | https://doi.org/10.1089/gtmb.2015.0014 | - |
dc.description.abstract | Aims: The Wnt planar cell polarity (PCP) pathway is one of the Wnt pathways which plays a critical role in cell proliferation and fate. The VANGL1 protein is one of Wnt-PCP pathway components. It is known that Wnt-PCP pathway has major roles in cell motility but its role in hepatocellular carcinoma (HCC) progression through invasion and metastasis needs to be clarified. Methods: We silenced VANGL1 gene expression in the HepG2 HCC cell line by stable transfection with a vector containing siRNA template for VANGL1 and investigated the change in cell invasion and motility. Results: Transfected cells with the siRNA template showed significantly suppressed invasive capacity when compared to controls although cellular motility was only slightly affected. Conclusion: Our study showed a basal role for VANGL1 with respect to the invasive capacity of HCC cells. This suggests that the Wnt-PCP pathway may play a role in progression of HCC through cellular invasion but further studies are needed to clarify its role in cell motility. © 2015, Mary Ann Liebert, Inc. | en_US |
dc.language.iso | en | en_US |
dc.publisher | Mary Ann Liebert Inc. | en_US |
dc.relation.ispartof | Genetic Testing and Molecular Biomarkers | en_US |
dc.rights | info:eu-repo/semantics/openAccess | en_US |
dc.subject | messenger RNA | en_US |
dc.subject | protein VANGL1 | en_US |
dc.subject | small interfering RNA | en_US |
dc.subject | unclassified drug | en_US |
dc.subject | Wnt protein | en_US |
dc.subject | carrier protein | en_US |
dc.subject | membrane protein | en_US |
dc.subject | VANGL1 protein, human | en_US |
dc.subject | Article | en_US |
dc.subject | cancer growth | en_US |
dc.subject | cell fate | en_US |
dc.subject | cell invasion | en_US |
dc.subject | cell motility | en_US |
dc.subject | cell polarity | en_US |
dc.subject | cell proliferation | en_US |
dc.subject | controlled study | en_US |
dc.subject | down regulation | en_US |
dc.subject | gene | en_US |
dc.subject | gene expression | en_US |
dc.subject | gene silencing | en_US |
dc.subject | genetic transfection | en_US |
dc.subject | HepG2 cell line | en_US |
dc.subject | human | en_US |
dc.subject | human cell | en_US |
dc.subject | liver cell carcinoma | en_US |
dc.subject | VANGL1 gene | en_US |
dc.subject | antagonists and inhibitors | en_US |
dc.subject | biosynthesis | en_US |
dc.subject | cell motion | en_US |
dc.subject | genetics | en_US |
dc.subject | Hep-G2 cell line | en_US |
dc.subject | liver tumor | en_US |
dc.subject | metabolism | en_US |
dc.subject | pathology | en_US |
dc.subject | physiology | en_US |
dc.subject | signal transduction | en_US |
dc.subject | tumor cell line | en_US |
dc.subject | tumor invasion | en_US |
dc.subject | Wnt signaling pathway | en_US |
dc.subject | Carcinoma, Hepatocellular | en_US |
dc.subject | Carrier Proteins | en_US |
dc.subject | Cell Line, Tumor | en_US |
dc.subject | Cell Movement | en_US |
dc.subject | Down-Regulation | en_US |
dc.subject | Gene Expression | en_US |
dc.subject | Hep G2 Cells | en_US |
dc.subject | Humans | en_US |
dc.subject | Liver Neoplasms | en_US |
dc.subject | Membrane Proteins | en_US |
dc.subject | Neoplasm Invasiveness | en_US |
dc.subject | RNA, Small Interfering | en_US |
dc.subject | Signal Transduction | en_US |
dc.subject | Transfection | en_US |
dc.subject | Wnt Signaling Pathway | en_US |
dc.title | Downregulation of VANGL1 inhibits cellular invasion rather than cell motility in hepatocellular carcinoma cells without stimulation | en_US |
dc.type | Article | en_US |
dc.identifier.volume | 19 | en_US |
dc.identifier.issue | 6 | en_US |
dc.identifier.startpage | 283 | |
dc.identifier.startpage | 283 | en_US |
dc.identifier.endpage | 287 | en_US |
dc.identifier.doi | 10.1089/gtmb.2015.0014 | - |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.identifier.pmid | 25874746 | en_US |
dc.identifier.scopus | 2-s2.0-84930890534 | en_US |
dc.identifier.wos | WOS:000363885000002 | en_US |
dc.identifier.scopusquality | Q2 | - |
dc.owner | Pamukkale University | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.grantfulltext | open | - |
item.languageiso639-1 | en | - |
item.openairetype | Article | - |
item.fulltext | With Fulltext | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | 14.02. Internal Medicine | - |
Appears in Collections: | PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection Tıp Fakültesi Koleksiyonu WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection |
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File | Size | Format | |
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Gökhan Ozan Çetin.pdf | 160.31 kB | Adobe PDF | View/Open |
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