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Received for publication May 5, 2006.
Revised July 4, 2006.
Accepted for publication July 11, 2006.
-ESTRADIOL, GENISTEIN AND 4-HYDROXYTAMOXIFEN INDUCE THE PROLIFERATION OF THYROID CANCER CELLS THROUGH THE G PROTEIN COUPLED-RECEPTOR GPR30
The higher incidence of thyroid carcinoma (TC) in women during reproductive years compared to men as well as the increased risk associated with the therapeutic use of estrogens have suggested a pathogenetic role exerted by these steroids in the development of TC. In the present study we have evaluated the potential of 17
-estradiol (E2), genistein (G) and 4-hydroxytamoxifen (OHT) to regulate the expression of diverse estrogen target genes as well as the proliferation of human WRO, FRO and ARO thyroid carcinoma cells, which were used as a model system. We have ascertained that ARO cells are devoid of ERs, whereas both WRO and FRO cells express a single variant of ER
which was neither transactivated, modulated nor translocated into the nucleus upon treatment with ligands. However, E2, G and OHT were able either to induce the transcriptional activity of c-fos promoter constructs, including that lacking the estrogen responsive elements (EREs), or to increase c-fos, cyclin A and D1 expression. Notably, we have demonstrated that the G protein-coupled receptor GPR30 and the MAPK pathway mediate both the up-regulation of c-fos and the growth response to E2, G and OHT in TC cells studied, since these stimulatory effects were prevented silencing GPR30 as well as using the MAPK inhibitor PD 98059. Our findings provide new insight into the molecular mechanisms through which estrogens may induce the progression of TC.
Key words:
Sex hormones, MAP Kinase, Immunocytochemistry, Regulation of gene expression
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