The activities of progesterone receptor isoform A and B are differentially modulated by their ligands in a gene-selective manner.

It is known that progesterone receptor (PR) isoform A (PR-A) and isoform B (PR-B) may mediate different effects of progesterone. The objective of this study was to determine if the functions of PR isoforms also vary in response to different PR modulators (PRM). The effects of 7 synthetic PRM were tested in MDA-MB-231 cells engineered to express PR-A, PR-B, or both PR isoforms.

Gene regulation profile reveals consistent anticancer properties of progesterone in hormone-independent breast cancer cells transfected with progesterone receptor.

Absence of estrogen receptor (ER) and progesterone receptor (PR) is the hallmark of most hormone-independent breast cancers. Previous studies demonstrated that reactivation of PR expression in hormone-independent MDA-MB-231 breast cancer cells enabled progesterone to suppress cell growth both in vitro and in vivo. We determined the whole genomic effect of progesterone in PR-transfected MDA-MB-231 cells.

Glucocorticoid and mineralocorticoid cross-talk with progesterone receptor to induce focal adhesion and growth inhibition in breast cancer cells.

Progesterone receptor (PR), glucocorticoid receptor, and mineralocorticoid receptor belong to a subfamily of nuclear receptor superfamily with similar sequence and structural characteristics. Many reports have documented glucocorticoid-like effects of progesterone in various tissues. This study addresses the issue of cross-talk between corticosteroids and PR using PR-transfected MDA-MB-231 cells ABC28 and vector-transfected control cells CTC15.