Induction of bcl-xL expression in mammary epithelial cells is glucocorticoid-dependent but not signal transducer and activator of transcription 5-dependent.
basic_science · Level V
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Abstract
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.
Medical subject headings
- DNA-Binding Proteins
- Dexamethasone
- Glucocorticoids
- Mammary Glands, Animal
- Milk Proteins
- Prolactin
- Proto-Oncogene Proteins c-bcl-2
- Receptors, Glucocorticoid
- Trans-Activators