| First Author | Tourneur L | Year | 2003 |
| Journal | Oncogene | Volume | 22 |
| Issue | 18 | Pages | 2795-804 |
| PubMed ID | 12743602 | Mgi Jnum | J:83474 |
| Mgi Id | MGI:2662071 | Doi | 10.1038/sj.onc.1206399 |
| Citation | Tourneur L, et al. (2003) Loss of FADD protein expression results in a biased Fas-signaling pathway and correlates with the development of tumoral status in thyroid follicular cells. Oncogene 22(18):2795-804 |
| abstractText | Downregulation of proapoptotic molecules like Fas or caspase 8, or upregulation of antiapoptotic molecules like FLICE inhibitory protein has been suggested to be a regulatory mechanism set up by tumor cells to block the death signal received via death receptors. In an in-depth study of the Fas/FasL-signaling pathway in thyroid tumor development, we have demonstrated that tumor cells specifically downregulate the multideath receptor adapter Fas-associated death domain (FADD). The regulation of FADD expression occurred only at the protein level. Furthermore, in the absence of FADD, Fas-signaling resulted in accelerated growth of thyrocytes. Since thyrocytes also acquired FasL expression during tumor development, the absence of FADD protein could lead to greater resistance to numerous death receptor-mediated apoptosis, stimulation of their own proliferation through Fas/FasL interaction, and the capacity to counter-attack the infiltrating lymphocytes. |
