title: MiR-195 inhibits proliferation and growth and induces apoptosis of endometrial stromal cells by targeting FKN.
abstract: MiR-195, which exhibits a proliferation-inhibiting role in different tumors, has been reported to be down-regulated in the ectopic endometrium. The aim of this study was to determine the impact of miR-195 on the biological characteristic of the endometrial stromal cells (ESCs). MiR-195 has been presumed to target the 3'-untranslated regions (3'-UTR) of Fractalkine (FKN), which also plays important roles in endometriosis. Fluorescence reporter assays showed that miR-195 effectively binds to the 3'-UTR of FKN. The normal ESCs showed a significant higher miR-195 expression than that of eutopic and ectopic ESCs associated with endometriosis, while the FKN expression showed opposite results. MiR-195 mimics inhibited proliferation and growth and induced apoptosis of eutopic ESCs, and these effects were abolished by FKN-siRNA. miR-195 could decrease the expression of survivin, matrix metalloproteinase-9 (MMP9) and up-regulate the expression of CD82, tissue inhibitor of metalloproteinase 1 (TIMP1) and TIMP2 of eutopic ESCs by targeting FKN. Our study has demonstrated for the first time that miR-195 plays important roles in regulating the functions of ESCs through targeting FKN. The information may be useful for developing a new therapeutic strategy for endometriosis.
authors.affiliation: Department of Assisted Reproductive, Shanghai Ninth Hospital Affiliated to JiaoTong University School of Medicine Shanghai, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Wang
authors.forename: Hong
authors.initials: H
authors.lastname: Chen
authors.forename: Yonglun
authors.initials: Y
authors.lastname: Fu
authors.forename: Ai
authors.initials: A
authors.lastname: Ai
authors.forename: Songguo
authors.initials: S
authors.lastname: Xue
authors.forename: Qifeng
authors.initials: Q
authors.lastname: Lyu
authors.forename: Yanping
authors.initials: Y
authors.lastname: Kuang
mesh_terms: D020413:3' Untranslated Regions; D000328:Adult; D017209:Apoptosis; D001665:Binding Sites; D016022:Case-Control Studies; D049109:Cell Proliferation; D002470:Cell Survival; D002478:Cells, Cultured; D054428:Chemokine CX3CL1 / Q000235:genetics / Q000378:metabolism*; D004715:Endometriosis / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D004717:Endometrium / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins / Q000378:metabolism; D051861:Kangai-1 Protein / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D034622:RNA Interference; D015398:Signal Transduction; D017154:Stromal Cells / Q000378:metabolism* / Q000473:pathology; D000077022:Survivin; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000378:metabolism; D019716:Tissue Inhibitor of Metalloproteinase-2 / Q000378:metabolism; D014162:Transfection
chemical_list: D020413:3' Untranslated Regions; C107489:BIRC5 protein, human; C497688:CD82 protein, human; C515538:CX3CL1 protein, human; D054428:Chemokine CX3CL1; D051034:Inhibitor of Apoptosis Proteins; D051861:Kangai-1 Protein; C552722:MIRN195 microRNA, human; D035683:MicroRNAs; D000077022:Survivin; C560822:TIMP1 protein, human; C560823:TIMP2 protein, human; D019715:Tissue Inhibitor of Metalloproteinase-1; D019716:Tissue Inhibitor of Metalloproteinase-2; C579270:MMP9 protein, human; D020780:Matrix Metalloproteinase 9
keywords: MiR-195; endometrial stromal cells; endometriosis; fractalkine