Estrogen-induced FOS like 1 regulates matrix metalloproteinase expression and the motility of human endometrial/decidual stromal cells [Cell Biology]

Estrogen-induced FOS like 1 regulates matrix metalloproteinase expression and the motility of human endometrial/decidual stromal cells [Cell Biology]: The regulation mechanisms involved in matrix metalloproteinase (MMP) expression and the motility of human endometrial/decidual stromal cells (ESCs/DSCs) during decidualization remain unclear. DSCs show a significant increased cell motility and expression of FOS like 1 (FOSL1) and MMP-1, -2, -9 when compared with ESCs, whereas a lack of decidualization inducers lead to a rapid decrease of FOSL1 and MMP-1, -9 expression in DSCs in vitro. Therefore, we hypothesized that a link exists between decidualization inducers and FOSL1 in the up-regulation of motility during decidualization. Detected based on the response of ESCs/DSCs to different decidualization systems in vitro, we found that progesterone (P4) alone exerted no significant effect and 17β-estradiol (E2) significantly increased cell motility and FOSL1, MMP-1, -9 expression at the mRNA and protein levels, whereas 8-Bromoadenosine 3’,5’-cyclic monophosphate (8-Br-cAMP) significantly decreased cell motility and FOSL1, MMP-9 expression in the presence of P4. In addition, we showed that E2 triggered the phosphorylation of estrogen receptor 1 (ESR1), which could directly bind to the promoter of FOSL1 in ESCs/DSCs. Additionally, we also revealed the silence of ESR1 expression by siRNA abrogated E2-induced FOSL1 expression at the transcript and protein levels. Moreover, the silence of FOSL1 expression by siRNA was able to block E2-induced MMP-1, -9 expression and cell motility in ESCs/DSCs. Taken together, our data suggests that, in addition to its enhancement of the secretory function, the change in MMP expression and cell motility is another component of the decidualization of ESCs/DSCs, including estrogen-dependent MMP-1, -9 expression mediated by E2-ESR1-FOSL1 signaling.