| Autor: |
Donckier, Julian E., Mertens-Strijthagen, Jeannine, Flamion, Bruno |
| Předmět: |
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| Zdroj: |
Clinical Endocrinology; Oct2007, Vol. 67 Issue 4, p552-556, 5p, 2 Black and White Photographs, 1 Graph |
| Abstrakt: |
Objective Endothelin-1 (ET-1) may play a role in carcinogenesis. ET-1 axis is overexpressed in thyroid carcinoma. We investigated the expression and the production of ET-1 by thyroid cancer cells as well as the effect of ET-1 receptor antagonism on cell proliferation. Design Human papillary and follicular thyroid carcinoma cell lines were cultured. Measurements (i) Prepro-ET-1, ET-1 receptors (ETA R and ETB R) and ET-1 converting enzyme (ECE) by reverse transcriptase polymerase chain reaction (RT-PCR); (ii) the presence of ETA R by western blot; (iii) ET-1 concentrations in medium by an enzyme immunometric assay; (iiii) the proliferation of cells by BrdU and tritiated thymidine incorporation. Results RT-PCR detected the presence of mRNA for prepro-ET-1, ETA R and ECE in papillary and follicular carcinoma cells. ETB R was only expressed by follicular cells. ETA R was also detected in both cell types by western blot. Measurements of ET-1 concentrations demonstrated a secretion of active ET-1 by the cells. ETA R antagonism with atrasentan reduced cell proliferation by 16% in papillary carcinoma cells ( P < 0·05) and by 51% in follicular carcinoma cells ( P < 0·001). Conclusions Papillary and follicular carcinoma cells express all components of the ET-1 axis. ETA R antagonism exerts antiproliferative effects, which opens up new therapeutic perspectives in thyroid carcinoma. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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