Estrogen-induced FOS-like 1 regulates matrix metalloproteinase expression and the motility of human endometrial and decidual stromal cells.

The regulation mechanisms involved in matrix metalloproteinase () expression and the motility of human endometrial and decidual stromal cells (ESCs and DSCs, respectively) during decidualization remain unclear. DSCs show significant increased cell motility and expression of FOS-like 1 () and , , and compared with ESCs, whereas lack of decidualization inducers leads to a rapid decrease in and and expression in DSCs Therefore, we hypothesized that a link exists between decidualization inducers and FOSL1 in up-regulation of motility during decidualization. Based on the response of ESCs/DSCs to different decidualization systems , we found that progesterone (P4) alone had no significant effect and that 17β-estradiol (E2) significantly increased cell motility and and and expression at the mRNA and protein levels, whereas 8-bromo-cAMP significantly decreased cell motility and and expression in the presence of P4. In addition, we showed that E2 triggered phosphorylation of estrogen receptor 1 (ESR1), which could directly bind to the promoter of in ESCs/DSCs. Additionally, we also revealed silencing of expression by siRNA abrogated E2-induced expression at the transcript and protein levels. Moreover, silencing of expression by siRNA was able to block E2-induced and expression and cell motility in ESCs/DSCs. Taken together, our data suggest that, in addition to its enhancement of secretory function, the change in expression and cell motility is another component of the decidualization of ESCs/DSCs, including estrogen-dependent and expression mediated by E2-ESR1-FOSL1 signaling.