Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2010) 22 P385

1Section of Endocrinology, Department of Biomedical Sciences and Advanced Therapies, University of Ferrara, Ferrara, Italy; 2Department of Medical and Surgical Science, General Surgery III, University of Padua, Padova, Italy; 3Section of General Surgery, Department of Surgery, University of Ferrara, Ferrara, Italy.


Pituitary tumour transforming gene 1 (PTTG1) is over-expressed in a variety of endocrine-related tumors. We investigated PTTG1 expression in human C-cell hyperplasia (CCH), human medullary thyroid carcinoma (MTC) and in the human MTC cell line, TT. PTTG1 expression was significantly higher (P<0.01) in CCH (threefold), in papillary thyroid cancer and in MTC (fivefold) than in normal thyroid, and in MTC lymph-node metastases as compared to primary lesions (approximately twofold; P<0.05). PTTG1 mRNA and protein correlated with tumor diameter and TNM status (P<0.05). In TT cells, PTTG1 silencing did not completely block DNA synthesis, but significantly reduced [3H]Thymidine incorporation (~50%; P<0.01) for up to 3 days. Furthermore, PTTG1 overexpression significantly decreased cell proliferation, lasting for at least 3 days (30–60%; P<0.01). Therefore, PTTG1 levels correlate with tumor aggressiveness. PTTG1 silencing and overexpression cause reduced MTC cell proliferation, supporting the hypothesis that PTTG1 is an important determinant of C-cell neoplastic proliferation.

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