There is accumulating evidence to suggest that progesterone
plays
an essential role in the regulation of growth and differentiation
of mammary glands and thus may
play a key role in breast cancer (Edwards, 2005). The biological response to progesterone is
mediated by two distinct forms
of the human progesterone receptor (PR-A and PR-B forms). In
most cell
contexts, the B form functions as a transcriptional activator, whereas the A form
functions as a transcriptional
inhibitor of steroid hormones (Attia et al., 2000; Lin et al., 2003).
Recently it has been demonstrated that there is differential hormone dependent regulation of the
phosphorylation of the A and B forms of the receptor (Clemm et al., 2000) . Treatment of T47D
breast cancer cells with progestin agonist increases the phosphorylation of Ser
190
and Ser
294
with different kinetics. These phosphorylation events may differentially affect the transcriptional
activity of the receptor.
