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

Vincenza Leone, Angelo Ferraro, Filippo Schepis, Antonella Federico, Romina Sepe, Claudio Arra, Concetta Langella, Giuseppe Palma, Carlo De Lorenzo, Giancarlo Troncone, Valeria Masciullo, Giovanni Scambia, Alfredo Fusco, Pierlorenzo Pallante

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)535-541
Number of pages7
JournalCancer Letters
Issue number2
Publication statusPublished - Feb 28 2015


  • Carcinoma
  • Cl2/dro1/ccdc80
  • Knock-out mice
  • Ovary
  • Thyroid

ASJC Scopus subject areas

  • Cancer Research
  • Oncology
  • Medicine(all)

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