Schorr K, Furth P A
Department of Physiology, University of Maryland Medical School, Baltimore 21201, USA.
Cancer Res. 2000 Nov 1;60(21):5950-3.
In the present study, we examined the role of prolactin and glucocorticoids in regulating bcl-x transcription in mammary epithelial cells. We report that dexamethasone, but not prolactin, induced native bcl-x gene expression in a dose-dependent manner in HC11 cells and enhanced serum-starved HC11 cell survival. This effect was mediated through the glucocorticoid receptor and independent of STAT-5 activity. We propose that the mechanism through which glucocorticoids enhance mammary epithelial cell survival is by increasing steady-state levels of bcl-xL, RNA.
在本研究中，我们检测了催乳素和糖皮质激素在调节乳腺上皮细胞中bcl-x转录方面的作用。我们报告，地塞米松而非催乳素，在HC11细胞中以剂量依赖方式诱导天然bcl-x基因表达，并提高血清饥饿的HC11细胞存活率。这种效应是通过糖皮质激素受体介导的，且独立于STAT-5活性。我们提出，糖皮质激素增强乳腺上皮细胞存活的机制是通过增加bcl-xL RNA的稳态水平。
