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The cl2/dro1/ccdc80 null mice develop thyroid and ovarian neoplasias

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The cl2/dro1/ccdc80 null mice develop thyroid

and ovarian neoplasias.

Leone V1, Ferraro A1, Schepis F2, Federico A1, Sepe R1, Arra C3, Langella C1, Palma G4, De Lorenzo C2, Troncone G5,

Masciullo V6, Scambia G6, Fusco A1, Pallante P7.

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Abstract

We have previously reported that the expression of the CL2/CCDC80 gene is downregulated in human papillary thyroid carcinomas, particularly in follicular variants. We have also reported that the restoration of CL2/CCDC80 expression reverted the malignant phenotype of thyroid carcinoma cell lines and that CL2/CCDC80 positively regulated E-cadherin expression, an ability that likely accounts for the role of the CL2/CCDC80 gene in thyroid cancer progression. In order to validate the tumour suppressor role of the CL2/CCDC80 gene in thyroid carcinogenesis we generated cl2/ccdc80 knock-out mice. We found that embryonic fibroblasts from cl2/ccdc80(-/-) mice showed higher proliferation rate and lower susceptibility to apoptosis. Furthermore, cl2/ccdc80(-/-) mice developed thyroid adenomas and ovarian

carcinomas. Finally, ret/PTC1 transgenic mice crossed with the cl2/ccdc80 knock-out mice developed more aggressive thyroid carcinomas compared with those observed in the single ret/PTC1 transgenic mice. Together, these results indicate CL2/CCDC80 as a putative tumour suppressor gene in human thyroid carcinogenesis.

Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

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