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dc.contributor.authorZeybek, N. Dilara
dc.contributor.authorGulcelik, Nese Ersoz
dc.contributor.authorKaymaz, F. Figen
dc.contributor.authorSarisozen, Can
dc.contributor.authorVural, Imran
dc.contributor.authorBodur, Ebru
dc.contributor.authorCanpinar, Hande
dc.contributor.authorUsman, Aydan
dc.contributor.authorAsan, Esin
dc.date.accessioned2019-12-12T06:25:58Z
dc.date.available2019-12-12T06:25:58Z
dc.date.issued2011
dc.identifier.issn0022-0795
dc.identifier.urihttps://doi.org/10.1530/JOE-10-0411
dc.identifier.urihttp://hdl.handle.net/11655/16336
dc.description.abstractStatins show antiproliferative activity in various cancer cells. The aim of this study was to evaluate the effects of rosuvastatin treatment on papillary thyroid carcinoma. The papillary thyroid carcinoma (B-CPAP) and normal (Nthy-ori 3-1) thyroid cell lines were treated with rosuvastatin at 12.5, 18.5, 25, 50, 100, and 200 mu M concentrations. After 48 and 72 h of rosuvastatin treatment, 3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide, Ki-67 immunolabeling, FACS analysis, electron microscopy, caspase-3, and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) analysis were performed. Decreased cell viability and G1 phase arrest were detected in papillary thyroid cell line treated with rosuvastatin. Positive immunoreactivity of Ki-67 and dose-dependent increase in S phase on Nthy-ori 3-1 cells were also detected. B-CPAP cells showed intense vacuolisation and autophagosomes with low concentrations and 48 h incubations, while Nthy-ori 3-1 cells showed these changes at higher concentrations. A decrease in the percentage of cells showing autophagy was determined with increasing concentrations of rosuvastatin in B-CPAP cells. Rosuvastatin treatment also caused a dose-and time-dependent increase in caspase-3 activity and apoptotic index by TUNEL assay in B-CPAP cells compared with the Nthy-ori 3-1 cells. Apoptotic cells with nuclear condensation and fragmentation were observed in B-CPAP cell line. Rosuvastatin induced autophagic changes in B-CPAP papillary thyroid cancer cells in lower doses and caused a shift from autophagy to apoptosis. Rosuvastatin may be an alternative treatment for refractory papillary thyroid cancer. Further in vivo studies are necessary to clarify the effects of rosuvastatin in papillary thyroid carcinoma and the clinical implications of rosuvastatin treatment. Journal of Endocrinology (2011) 210, 105-115
dc.language.isoen
dc.publisherBioscientifica Ltd
dc.relation.isversionof10.1530/JOE-10-0411
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectEndocrinology & Metabolism
dc.titleRosuvastatin Induces Apoptosis in Cultured Human Papillary Thyroid Cancer Cells
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.relation.journalJournal Of Endocrinology
dc.contributor.departmentHistoloji ve Embriyoloji
dc.identifier.volume210
dc.identifier.issue1
dc.identifier.startpage105
dc.identifier.endpage115
dc.description.indexWoS
dc.description.indexScopus


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