dc.creatorKohan Ivani, Karla
dc.creatorGabler Neale, Fernando
dc.creatorSelman,
dc.creatorVega Blanco, María Margarita
dc.creatorRomero Osses, Carmen
dc.date.accessioned2019-03-18T11:53:43Z
dc.date.available2019-03-18T11:53:43Z
dc.date.created2019-03-18T11:53:43Z
dc.date.issued2016
dc.identifierJournal of Cancer Research and Clinical Oncology, Volumen 142, Issue 1, 2018, Pages 47-58
dc.identifier14321335
dc.identifier01715216
dc.identifier10.1007/s00432-015-1998-y
dc.identifierhttps://repositorio.uchile.cl/handle/2250/166712
dc.description.abstract© 2015, The Author(s).Purpose: 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-β1 pathway that might modify the anti-proliferative effect of the latter. Methods: The levels of TGF-β1 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-β1 and DHT + TGF-β1 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 immunocyt
dc.languageen
dc.publisherSpringer Verlag
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.sourceJournal of Cancer Research and Clinical Oncology
dc.subjectAndrogen receptor
dc.subjectEpithelial ovarian cancer
dc.subjectTGF-β signaling pathway
dc.titleRole of dihydrotestosterone (DHT) on TGF-β1 signaling pathway in epithelial ovarian cancer cells
dc.typeArtículos de revistas


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