{"paper_id":"03c626f5-0ed3-4521-8ac5-f3335f91418b","body_text":"Abstract\nEndometriosis is a frequent gynecological disease associated with severe pain and infertility.\nAlthough its dependency on estrogen is well recognized, the molecular mechanism along the estrogenic\npathway has not been fully understood. This study investigates the effect of 17β-estradiol (E2) on human\nendometrial stromal cell (HESC) invasion and the role of c-fos and matrix metalloproteinase-9 (MMP-9) in\nmediating the biological function of 17β-E2. It is found that 17β-E2 promotes not only HESC invasion, but also\nc-fos and MMP-9 expression in HESC. Further experiments demonstrate that the estrogen receptor inhibitor\nICI 182780 and siRNA-mediated c-fos or MMP-9 knockdown are able to block the effect of 17β-E2 on HESC\ninvasion. Moreover, siRNA-mediated c-fos knockdown suppresses the effect of 17β-E2 on MMP-9 expression.\nOur results indicate that 17β-E2-induced HESC invasion is dependent on c-fos-mediated MMP-9 expression.\nThese findings facilitate our understanding on the pathogenesis of endometriosis and may provide data\npotentially useful for the development of new treatment modalities for better management of endometriosis.\nKeywords: 17β-estradiol, human endometrial stromal cell, c-fos, MMP-9, invasion.\n52\n5","source_license":"CC0","license_restricted":false}