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Induction of bcl-x_L Expression in Mammary Epithelial Cells Is Glucocorticoid-dependent but not Signal Transducer and Activator of Transcription 5-dependent¹

Department of Physiology [K. S., P. A. F.], and Institute of Human Virology and Division of Infectious Disease, Department of Medicine [P. A. F.], University of Maryland Medical School, Baltimore, Maryland 21201

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-x_L RNA.

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