| First Author | Leone V | Year | 2015 |
| Journal | Cancer Lett | Volume | 357 |
| Issue | 2 | Pages | 535-41 |
| PubMed ID | 25497869 | Mgi Jnum | J:217742 |
| Mgi Id | MGI:5615523 | Doi | 10.1016/j.canlet.2014.12.010 |
| Citation | Leone V, et al. (2015) The cl2/dro1/ccdc80 null mice develop thyroid and ovarian neoplasias. Cancer Lett 357(2):535-41 |
| abstractText | 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. |
