c-Fos-Regulated Matrix Metalloproteinase-9 Expression is Involved in 17β-Estradiol-Promoted Invasion of Human Endometrial Stromal Cell

Hai-Yang Pan, H Pan, Pan H, Zhang P, P Zhang, Li JR, J.-R. Li, H Wang, Wang H, M-F Jin, Jin MF, Ming-shun Jin, C Feng, Feng Cheng, Feng C, He‐Feng Huang, Huang HF, Hefeng Huang, H-F Huang
Current Molecular Medicine · 2016 · vol. 16(3) , pp. 266–275 · doi:10.2174/1566524016666160225153454 · PMID:26917263 · W2282726358
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17β-estradiol promotes human endometrial stromal cell invasion by upregulating c-Fos and matrix metalloproteinase-9 expression.

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⚙ AI-generated deep summary by claude@2026-07, 2026-07-09 · read from full text ⓘ

The paper studied how 17β-estradiol (E2) affects invasion of human endometrial stromal cells (HESC) and examined whether the pathway involves c-fos and matrix metalloproteinase-9 (MMP-9). Using experiments in HESC, the authors found that E2 promotes invasion while also increasing c-fos and MMP-9 expression, and that blocking estrogen signaling with the receptor inhibitor ICI 182780 prevents these E2 effects. They further reported that siRNA knockdown of c-fos or MMP-9 blocks E2-driven HESC invasion, and that c-fos knockdown also suppresses the E2-induced MMP-9 expression. This study is centrally about endometriosis — it investigates an estrogen-dependent molecular mechanism (c-fos→MMP-9) underlying endometrial stromal invasion relevant to endometriosis pathogenesis.

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Abstract

Endometriosis is a frequent gynecological disease associated with severe pain and infertility. Although its dependency on estrogen is well recognized, the molecular mechanism along the estrogenic pathway has not been fully understood. This study investigates the effect of 17β-estradiol (E2) on human endometrial stromal cell (HESC) invasion and the role of c-fos and matrix metalloproteinase-9 (MMP-9) in mediating the biological function of 17β-E2. It is found that 17β-E2 promotes not only HESC invasion, but also c-fos and MMP-9 expression in HESC. Further experiments demonstrate that the estrogen receptor inhibitor ICI 182780 and siRNA-mediated c-fos or MMP-9 knockdown are able to block the effect of 17β-E2 on HESC invasion. Moreover, siRNA-mediated c-fos knockdown suppresses the effect of 17β-E2 on MMP-9 expression. Our results indicate that 17β-E2-induced HESC invasion is dependent on c-fos-mediated MMP-9 expression. These findings facilitate our understanding on the pathogenesis of endometriosis and may provide data potentially useful for the development of new treatment modalities for better management of endometriosis.
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Abstract

Endometriosis is a frequent gynecological disease associated with severe pain and infertility. Although its dependency on estrogen is well recognized, the molecular mechanism along the estrogenic pathway has not been fully understood. This study investigates the effect of 17β-estradiol (E2) on human endometrial stromal cell (HESC) invasion and the role of c-fos and matrix metalloproteinase-9 (MMP-9) in mediating the biological function of 17β-E2. It is found that 17β-E2 promotes not only HESC invasion, but also c-fos and MMP-9 expression in HESC. Further experiments demonstrate that the estrogen receptor inhibitor ICI 182780 and siRNA-mediated c-fos or MMP-9 knockdown are able to block the effect of 17β-E2 on HESC invasion. Moreover, siRNA-mediated c-fos knockdown suppresses the effect of 17β-E2 on MMP-9 expression. Our results indicate that 17β-E2-induced HESC invasion is dependent on c-fos-mediated MMP-9 expression. These findings facilitate our understanding on the pathogenesis of endometriosis and may provide data potentially useful for the development of new treatment modalities for better management of endometriosis.

Keywords

17β-estradiol, human endometrial stromal cell, c-fos, MMP-9, invasion. 52 5

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Condition tags

endometriosisinfertility

MeSH descriptors

Endometriosis Endometrium Estradiol Matrix Metalloproteinase 9 Proto-Oncogene Proteins c-fos Stromal Cells Adult Adult Cell Movement Cell Movement Cell Movement Endometriosis Endometriosis Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Estradiol

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