Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 22 P810

ECE2010 Poster Presentations Thyroid (122 abstracts)

Atorvastatin inhibited proliferation in papillary thyroid cancer cell line

Nese Ersoz Gulcelik 1 , Dilara Zeybek 2 , Figen Kaymaz 2 , Can Sarisozen 3 , Esin Asan 2 , Imran Vural 3 & Aydan Usman 1

1Department of Endocrinology and Metabolism, Hacettepe University Medical School, Ankara, Turkey; 2Department of Histology and Embryology, Hacettepe University Medical School, Ankara, Turkey; 3Hacettepe University Faculty of Pharmacy, Ankara, Turkey.

Aim: The role of statins on thyroid cell proliferation is of clinical interest. In this study, we investigated the effect of atorvastatin on papillary thyroid cell line (B-CPAP) and normal thyroid (Nthy-ori3-1) cell lines.

Materials and methods: In this in vitro study, B-CPAP and Nthy-ori3-1 cell lines were treated with atorvastatin at 12.5, 25, 50, 100, 200 μM concentrations. At 48 and 72 h MTT, electron microscopy and immunohistochemistry were performed.

Results: Atorvastatin treatment at different concentrations of 12.5 μM to 200 μM resulted in increased cell death of B-CPAP cells after 48 and 72 h (72.1 to 98.7% and 97.0 to 98.8%, respectively). Atorvastatin treatment at the same concentrations resulted in death of Nthy-ori3-1 cells after 48 and 72 h (39.6 to 94.2% and 57.7 to 98.0%, respectively). We observed euchromatic nucleus, prominent nucleolus and normal RER, ribosomes, mitochondria, glycogen in the cytoplasm of control groups of both cell lines. In atorvastatin treated cell lines the ratio of the cells with cytoplasmic vaculozations and chromatin condensations was increased. We also observed an increase in the number of apoptotic cells with chromatin condensation and cytoplasmic blebbing in higher treatment doses in both cell lines. Beside apoptotic cells, we also observed mitotic cells in normal thyroid cell line. This data was confirmed with positive immunoreactivity of Ki-67 on normal thyroid cells. However, mitotic cells weren’t detected in B-CPAP cells treated with different doses and intervals of atorvastatin.

Conclusion: Atorvastatin yielded cell death in both normal thyroid cells and papillary thyroid cancer cells. Atorvastatin inhibited proliferation of papillary thyroid cancer cells. This inhibition wasn’t seen in normal thyroid cells. Atorvastatin treatment may be of clinical use in patients with papillary thyroid cancer, particularly in metastatic patients. Clinical implications of these findings need to be tested by in vivo studies.

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