Suppression of Nuclear Factor-κB by Glucocorticoid Receptor Blocks Estrogen-Induced Apoptosis in Estrogen-Deprived Breast Cancer Cells.

ABSTRACT: Our clinically relevant finding is that glucocorticoids block estrogen (E₂)-induced apoptosis in long-term E₂-deprived (LTED) breast cancer cells. However, the mechanism remains unclear. Here, we demonstrated that E₂ widely activated adipose inflammatory factors such as fatty acid desaturase 1 (FADS1), IL6, and TNFα in LTED breast cancer cells. Activation of glucocorticoid receptor (GR) by the synthetic glucocorticoid dexamethasone upregulated FADS1 and IL6, but downregulated TNFα expression. Furthermore, dexamethasone was synergistic or additive with E₂ in upregulating FADS1 and IL6 expression, whereas it selectively and constantly suppressed TNFα expression induced by E₂ in LTED breast cancer cells. Regarding regulation of endoplasmi

SUBMITTER: Fan P 

PROVIDER: S-EPMC6774891 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature