title: MicroRNA23a and microRNA23b deregulation derepresses SF-1 and upregulates estrogen signaling in ovarian endometriosis.
abstract: BACKGROUND
  Steroidogenic factor (SF)-1 and its downstream target genes involved in estrogen signaling are aberrantly expressed in ovarian endometriosis.
  
  
  OBJECTIVE
  Our objective was to explore the microRNA-mediated mechanism controlling aberrant SF-1 expression in ovarian endometriosis.
  
  
  METHODS
  Bioinformatics analysis predicted that microRNA23a and microRNA23b (miR23a/b) target the NR5A1 3'-untranslated region. We investigated the relative expression and spatial distribution of miR23a/b and analyzed the relationship between miR23a/b and SF-1 expression in endometriotic tissues.
  
  
  METHODS
  The study was conducted at the Department of Gynecology and Obstetrics, West China Second University Hospital of Sichuan University.
  
  
  METHODS
  We enrolled 23 women with American Fertility Society stage III-IV ovarian endometriosis and 15 disease-free control subjects.
  
  
  METHODS
  Quantitative real-time RT-PCR, in situ hybridization, cell culture, transfections, and luciferase reporter assays were used in this study.
  
  
  METHODS
  The expression of miR23a/b and SF-1, CYP19A1, and StAR mRNAs; the relationships between miRNAs and SF-1 mRNA levels; and the effect of miR23a/b on SF-1 expression were measured in normal and eutopic endometrial stromal cells (ESCs) and 293T cells.
  
  
  RESULTS
  Both miR23a and miR23b were downregulated in ectopic and eutopic endometrium, compared with normal endometrium, and their expression was inversely correlated with NR5A1 mRNA levels. SF-1 expression was inhibited by miR23a/b overexpression in eutopic ESCs and upregulated by miR23a/b inhibition in normal ESCs.
  
  
  CONCLUSIONS
  MiR23a and miR23b are potential biomarkers of ovarian endometriosis. This study provides a novel approach for targeting the mechanisms controlling aberrant local estrogen biosynthesis in endometriosis.
authors: Department of Obstetrics and Gynecology, West China Second University Hospital of Sichuan University, No. 20 Section 3 Renmin South Road, Chengdu Sichuan 610041, PR China.
authors: Licong
authors: L
authors: Shen
authors: Shiyuan
authors: S
authors: Yang
authors: Wei
authors: W
authors: Huang
authors: Wenming
authors: W
authors: Xu
authors: Qiushi
authors: Q
authors: Wang
authors: Yong
authors: Y
authors: Song
authors: Ying
authors: Y
authors: Liu
mesh_terms: D000328:Adult; D002478:Cells, Cultured; D004715:Endometriosis / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D063185:Epigenetic Repression / Q000235:genetics; D004967:Estrogens / Q000378:metabolism / Q000494:pharmacology*; D005260:Female; D005786:Gene Expression Regulation / Q000502:physiology; D057809:HEK293 Cells; D006801:Humans; D035683:MicroRNAs / Q000235:genetics* / Q000502:physiology; D010049:Ovarian Diseases / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction / Q000187:drug effects / Q000235:genetics; D054339:Steroidogenic Factor 1 / Q000235:genetics*; D017154:Stromal Cells / Q000378:metabolism / Q000473:pathology; D014162:Transfection; D015854:Up-Regulation / Q000235:genetics / Q000502:physiology; D055815:Young Adult
chemical_list: D004967:Estrogens; C552430:MIRN23a microRNA, human; D035683:MicroRNAs; D054339:Steroidogenic Factor 1