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Authordc.contributor.authorKohan Ivani, Karla 
Authordc.contributor.authorGabler Neale, Fernando 
Authordc.contributor.authorSelman Abuchaibe, Alberto 
Authordc.contributor.authorVega Blanco, María Margarita 
Authordc.contributor.authorRomero Osses, Carmen 
Cita de ítemdc.identifier.citationJ Cancer Res Clin Oncol (2016) 142:47–58en_US
Identifierdc.identifier.otherDOI: 10.1007/s00432-015-1998-y
General notedc.descriptionArtículo de publicación ISIen_US
Abstractdc.description.abstractPurpose One of the hypotheses regarding the genesis of epithelial ovarian cancer involves the action of androgens on the proliferation of epithelial ovarian cells, as well as inclusion cysts. The purpose of the present study was to evaluate whether DHT causes changes in the TGF-beta 1 pathway that might modify the anti-proliferative effect of the latter. Methods The levels of TGF-beta 1 protein, of its receptors (TGFBR1 and TGFBR2), of Smad2/3 (canonical signaling pathway protein) and of p21 (cell cycle protein) were assessed in ovarian tissues, epithelial ovarian cancer cell lines (A2780) and control cell lines (HOSE) through the use of immunohistochemistry and immunocytochemistry. Additionally, cell lines were treated with 100 nmol/L DHT, 10 ng/mL of TGF-beta 1 and DHT + TGF-beta 1 during 72 h in the presence and absence of a siRNA against androgen receptor. After treatment, TGFBR1 and TGFBR2 levels were detected through Western blotting and p21 was assessed through immunocytochemistry. Results Epithelial ovarian cancer tissues showed a decrease in TGF-beta 1 I receptor (p < 0.05) and a change in Smad2/3 protein levels. Additionally, after treatment of cell lines with DHT, protein levels of TGF-beta 1 receptors (TGFBR1-TGFBR2) showed a decrease (p < 0.05) that might cause a potential disorder in TGF-beta 1 response, represented by the significant decrease in p21 protein levels in the presence of DHT (p < 0.001). Conclusions Overall, our results indicate a defect in the canonical TGF-beta signaling pathway in epithelial ovarian cancer caused by androgen action, thus suggesting eventual changes in such tissue proliferation rates.en_US
Patrocinadordc.description.sponsorshipGrant FODECYT 1110372; Proyect CONICYT FONDAP 15130011; CONICYTen_US
Type of licensedc.rightsAtribución-NoComercial-SinDerivadas 3.0 Chile*
Link to Licensedc.rights.uri*
Keywordsdc.subjectEpithelial ovarian canceren_US
Keywordsdc.subjectAndrogen receptoren_US
Keywordsdc.subjectTGF-beta signaling pathwayen_US
Títulodc.titleRole of dihydrotestosterone (DHT) on TGF‑β1 signaling pathway in epithelial ovarian cancer cellsen_US
Document typedc.typeArtículo de revistaen_US

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Atribución-NoComercial-SinDerivadas 3.0 Chile
Except where otherwise noted, this item's license is described as Atribución-NoComercial-SinDerivadas 3.0 Chile