title: MiR-23b targets cyclin G1 and suppresses ovarian cancer tumorigenesis and progression.
abstract: BACKGROUND
  It has been proposed that cyclin G1 (CCNG1) participates in p53-dependent G1-S and G2 checkpoints and might function as an oncogenic protein in the initiation and metastasis of ovarian carcinoma. MicroRNA 23b (miR-23b) is a critical regulatory factor in the progression of many cancer cell types that targets the relevant genes.
  
  
  METHODS
  MiR-23b expression in ovarian tissues was quantified by quantitative reverse transcription-PCR. The ovarian cancer cell lines OVCAR3, HO8910-PM, and SKOV3/DDP were transfected with miR-23b, after we assayed the cell phenotype and expression of the relevant molecules. Dual-luciferase reporter assay and a xenograft mouse model were used to examine the expression of miR-23b and its target gene CCNG1.
  
  
  RESULTS
  MIR23B mRNA expression was significantly lower in epithelial ovarian carcinoma and borderline tumors than in normal ovarian tissues and benign tumors, and miR-23b expression among ages and pathological subtypes was significantly different. CCNG1 mRNA expression was significantly lower in normal ovarian tissues than in benign tumors, borderline tumors, and ovarian carcinomas, and expression among pathological subtypes was significantly different. MiR-23b overexpression inhibited ovarian cancer cell proliferation, invasion, and migration, and induced apoptosis. Dual-luciferase reporter assay showed that miR-23b bound with the 3' untranslated region of CCNG1. MiR-23b overexpression significantly downregulated CCNG1, urokinase, survivin, Bcl-xL, P70S6K, and matrix metallopeptidase-9 (MMP9) mRNA and protein expression. Furthermore, miR-23b inhibited tumor growth and suppressed CCNG1 expression in vitro.
  
  
  CONCLUSIONS
  Our findings show that miR-23b may inhibit ovarian cancer tumorigenesis and progression by downregulating CCNG1 and the expression of the relevant genes. MiR-23b is a potentially novel application for regulating ovarian carcinoma progression.
authors.affiliation: Department of Biochemistry and Molecular Biology, College of Basic Medicine, China Medical University, 100013, Shenyang, China. yanjing-cmu@163.com.
authors.forename: Jing
authors.initials: J
authors.lastname: Yan
authors.affiliation: Department of Biochemistry and Molecular Biology, College of Basic Medicine, China Medical University, 100013, Shenyang, China. 771277967@qq.com.
authors.forename: Jing-yi
authors.initials: JY
authors.lastname: Jiang
authors.affiliation: Department of Biochemistry and Molecular Biology, College of Basic Medicine, China Medical University, 100013, Shenyang, China. Idcu1230@hotmail.com.
authors.forename: Xiao-Na
authors.initials: XN
authors.lastname: Meng
authors.affiliation: Department of Gynecology, The First Affiliated Hospital of China Medical University, 110001, Shenyang, China. xiuyinling@126.com.
authors.forename: Yin-Ling
authors.initials: YL
authors.lastname: Xiu
authors.affiliation: Department of Biochemistry and Molecular Biology, College of Basic Medicine, China Medical University, 100013, Shenyang, China. zongzhi_999@163.com.
authors.forename: Zhi-Hong
authors.initials: ZH
authors.lastname: Zong
mesh_terms: D020413:3' Untranslated Regions; D000818:Animals; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D056766:Cyclin G1 / Q000235:genetics*; D015536:Down-Regulation; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D051379:Mice; D035683:MicroRNAs / Q000235:genetics*; D009368:Neoplasm Transplantation; D010051:Ovarian Neoplasms / Q000235:genetics* / Q000473:pathology*; D011379:Prognosis
chemical_list: D020413:3' Untranslated Regions; C534702:CCNG1 protein, human; D056766:Cyclin G1; C552430:MIRN23a microRNA, human; D035683:MicroRNAs