Abstract
BackgroundIt 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.MethodsMiR-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.ResultsMIR23B 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.ConclusionsOur 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.
Highlights
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
Our previous study showed that MicroRNA 23b (miR-23b) was highly expressed in normal ovarian tissues than ovarian carcinoma tissues, and our predicted seed region in the 3′ untranslated regions (3′ UTR) of CCNG1 revealed that it’s a target of miR23b, we investigated the involvement of CCNG1 and miR-23b in ovarian cancer for the first time
CCNG1 mRNA expression was significantly lower in the normal ovarian tissues and benign ovarian tumors than in the ovarian carcinomas (Fig. 1e, p < 0.05)
Summary
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. The incidence of ovarian cancer is perpetually high: 200,000 new cases are diagnosed annually worldwide. Each year, it constitutes 4 % of all cancers diagnosed in women, and there are 6.6 new cases per 100,000 women per year [1, 2]. Ovarian cancer caused 160,500 deaths in 2010, an increase from the 113,600 in 1990 and the 140,200 in 2008 [3, 4]. MicroRNAs (miRNAs) are a class of small non-coding RNAs that negatively regulate gene expression at posttranscriptional level [7]. It has been demonstrated that a small number of miRNAs actively participate in regulating tumor development; it has been shown that they play different roles in different organs, relating to. Our previous study showed that miR-23b was highly expressed in normal ovarian tissues than ovarian carcinoma tissues, and our predicted seed region in the 3′ untranslated regions (3′ UTR) of CCNG1 revealed that it’s a target of miR23b, we investigated the involvement of CCNG1 and miR-23b in ovarian cancer for the first time
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