Kulasingam Vathany, Diamandis Eleftherios P
Department of Laboratory Medicine and Pathobiology, University of Toronto, and Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto M5G 1X5, ON, Canada.
Biol Chem. 2007 Oct;388(10):1113-9. doi: 10.1515/BC.2007.103.
Using the breast cell lines MCF-10A, MDA-MB-468 and T-47D, we investigated the role of various glucocorticoids in regulating human kallikrein 10 expression. We found that increased concentrations of glucocorticoids decreased KLK10 expression in MCF-10A and increased KLK10 expression in MDA-MB-468 and T-47D cells. Stimulation of the cell lines using other steroid hormones did not yield any difference in KLK10 expression in MCF-10A and MDA-MB-468 cells, suggesting that regulation of KLK10 occurs primarily through glucocorticoids. However, T-47D cells expressed higher levels of KLK10 upon dihydrotestosterone stimulation. Blocking the glucocorticoid receptor (GR) demonstrated that the mechanisms of induction and repression are different in the three cell lines studied. Taken together, our results suggest an alternative mode of KLK10 regulation - by glucocorticoids via GR-dependent mechanisms.
我们使用乳腺细胞系MCF-10A、MDA-MB-468和T-47D，研究了各种糖皮质激素在调节人激肽释放酶10表达中的作用。我们发现，糖皮质激素浓度升高会降低MCF-10A中的KLK10表达，并增加MDA-MB-468和T-47D细胞中的KLK10表达。使用其他类固醇激素刺激细胞系，MCF-10A和MDA-MB-468细胞中的KLK10表达没有任何差异，这表明KLK10的调节主要通过糖皮质激素进行。然而，双氢睾酮刺激后，T-47D细胞中KLK10表达水平更高。阻断糖皮质激素受体（GR）表明，在所研究的三种细胞系中，诱导和抑制机制不同。综上所述，我们的结果提示了一种KLK10调节的替代模式——糖皮质激素通过GR依赖机制进行调节。
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