PMID- 31937587 OWN - NLM STAT- MEDLINE DCOM- 20201014 LR - 20210317 IS - 1083-351X (Electronic) IS - 0021-9258 (Print) IS - 0021-9258 (Linking) VI - 295 IP - 8 DP - 2020 Feb 21 TI - Estrogen-induced FOS-like 1 regulates matrix metalloproteinase expression and the motility of human endometrial and decidual stromal cells. PG - 2248-2258 LID - S0021-9258(17)48263-9 [pii] LID - 10.1074/jbc.RA119.010701 [doi] AB - The regulation mechanisms involved in matrix metalloproteinase (MMP) 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 (FOSL1) and MMP1, MMP2, and MMP9 compared with ESCs, whereas lack of decidualization inducers leads to a rapid decrease in FOSL1 and MMP1 and MMP9 expression in DSCs in vitro 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 in vitro, we found that progesterone (P4) alone had no significant effect and that 17beta-estradiol (E2) significantly increased cell motility and FOSL1 and MMP1 and MMP9 expression at the mRNA and protein levels, whereas 8-bromo-cAMP significantly decreased cell motility and FOSL1 and MMP9 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 FOSL1 in ESCs/DSCs. Additionally, we also revealed silencing of ESR1 expression by siRNA abrogated E2-induced FOSL1 expression at the transcript and protein levels. Moreover, silencing of FOSL1 expression by siRNA was able to block E2-induced MMP1 and MMP9 expression and cell motility in ESCs/DSCs. Taken together, our data suggest that, in addition to its enhancement of secretory function, the change in MMP expression and cell motility is another component of the decidualization of ESCs/DSCs, including estrogen-dependent MMP1 and MMP9 expression mediated by E2-ESR1-FOSL1 signaling. CI - (c) 2020 Chen et al. FAU - Chen, Chao AU - Chen C AD - Department of Obstetrics and Gynecology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China; Shanghai Key Laboratory of Gynecologic Oncology, Shanghai 200127, China. FAU - Li, Congcong AU - Li C AD - Department of Obstetrics and Gynecology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China; Shanghai Key Laboratory of Gynecologic Oncology, Shanghai 200127, China. FAU - Liu, Weichun AU - Liu W AD - Department of Obstetrics and Gynecology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China. FAU - Guo, Feng AU - Guo F AD - Department of Obstetrics and Gynecology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China; Shanghai Key Laboratory of Gynecologic Oncology, Shanghai 200127, China. FAU - Kou, Xi AU - Kou X AD - Department of Obstetrics and Gynecology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China. FAU - Sun, Si AU - Sun S AD - Department of Obstetrics and Gynecology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China. FAU - Ye, Taiyang AU - Ye T AD - Department of Obstetrics and Gynecology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China. FAU - Li, Shanji AU - Li S AD - Department of Obstetrics and Gynecology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China. FAU - Zhao, Aimin AU - Zhao A AD - Department of Obstetrics and Gynecology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China; Shanghai Key Laboratory of Gynecologic Oncology, Shanghai 200127, China. Electronic address: zamzkh0526@126.com. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20200114 PL - United States TA - J Biol Chem JT - The Journal of biological chemistry JID - 2985121R RN - 0 (Estrogen Receptor alpha) RN - 0 (Estrogens) RN - 0 (IGFBP1 protein, human) RN - 0 (Insulin-Like Growth Factor Binding Protein 1) RN - 0 (Proto-Oncogene Proteins c-fos) RN - 0 (fos-related antigen 1) RN - 9002-62-4 (Prolactin) RN - EC 3.4.24.- (Matrix Metalloproteinases) SB - IM MH - Adult MH - *Cell Movement/drug effects MH - Decidua/*cytology MH - Endometrium/*cytology MH - Estrogen Receptor alpha/metabolism MH - Estrogens/*pharmacology MH - Female MH - Humans MH - Insulin-Like Growth Factor Binding Protein 1/metabolism MH - Matrix Metalloproteinases/*metabolism MH - Middle Aged MH - Prolactin/metabolism MH - Proto-Oncogene Proteins c-fos/*metabolism MH - Stromal Cells/cytology/drug effects/enzymology MH - Young Adult PMC - PMC7039546 OTO - NOTNLM OT - FOS-like 1 OT - cell invasion OT - cell migration OT - decidualization OT - estrogen OT - estrogen receptor OT - human decidual stromal cells OT - human endometrial stromal cells OT - matrix metalloproteinase (MMP) COIS- The authors declare that they have no conflicts of interest with the contents of this article EDAT- 2020/01/16 06:00 MHDA- 2020/10/21 06:00 PMCR- 2021/02/21 CRDT- 2020/01/16 06:00 PHST- 2019/08/18 00:00 [received] PHST- 2020/01/01 00:00 [revised] PHST- 2020/01/16 06:00 [pubmed] PHST- 2020/10/21 06:00 [medline] PHST- 2020/01/16 06:00 [entrez] PHST- 2021/02/21 00:00 [pmc-release] AID - S0021-9258(17)48263-9 [pii] AID - RA119.010701 [pii] AID - 10.1074/jbc.RA119.010701 [doi] PST - ppublish SO - J Biol Chem. 2020 Feb 21;295(8):2248-2258. doi: 10.1074/jbc.RA119.010701. Epub 2020 Jan 14.