Background: Pituitary tumour transforming gene 1 (PTTG1) is over-expressed in a variety of endocrine-related tumors. We aimed at evaluating PTTG1 expression and function in human neoplastic parafollicular C cells, represented by medullary thyroid carcinoma (MTC) and C-cell hyperplasia (CCH) samples and by the TT cell line. Methods: TT cells and tissues derived from human CCH and MTC were analyzed by northern blot, furthermore TT cells were subjected to PTTG gene silencing and cells were analyzed for DNA synthesis. Results: PTTG1 expression was significantly higher (P<0.01) in CCH (3-fold), in papillary thyroid cancer and in MTC (5-fold) than in normal thyroid, and in MTC lymph-node metastases as compared to primary lesions (~2-fold; 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. Conclusions: PTTG1 levels correlate with tumor aggressiveness. PTTG1 silencing causes reduced MTC cell proliferation, supporting the hypothesis that PTTG1 might have an important role in C-cell neoplastic proliferation.
Role of Piuitary Tumour Transforming Gene 1 in medullary thyroid carcinoma
ZATELLI, Maria Chiara;TAGLIATI, Federico;AMODIO, Vincenzo;Buratto M.;PANSINI, Giancarlo;BONDANELLI, Marta;AMBROSIO, Maria Rosaria;DEGLI UBERTI, Ettore
2010
Abstract
Background: Pituitary tumour transforming gene 1 (PTTG1) is over-expressed in a variety of endocrine-related tumors. We aimed at evaluating PTTG1 expression and function in human neoplastic parafollicular C cells, represented by medullary thyroid carcinoma (MTC) and C-cell hyperplasia (CCH) samples and by the TT cell line. Methods: TT cells and tissues derived from human CCH and MTC were analyzed by northern blot, furthermore TT cells were subjected to PTTG gene silencing and cells were analyzed for DNA synthesis. Results: PTTG1 expression was significantly higher (P<0.01) in CCH (3-fold), in papillary thyroid cancer and in MTC (5-fold) than in normal thyroid, and in MTC lymph-node metastases as compared to primary lesions (~2-fold; 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. Conclusions: PTTG1 levels correlate with tumor aggressiveness. PTTG1 silencing causes reduced MTC cell proliferation, supporting the hypothesis that PTTG1 might have an important role in C-cell neoplastic proliferation.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
