Endometriosis Knowledgebase


A repository for genes associated with endometriosis

Results


PMID 23450049
Gene Name MIR23B
Condition Endometriosis (ovarian)
Association Associated
Sex Female
Associated genes miR23a, miR23b
Other associated phenotypes Endometriosis
MicroRNA23a and microRNA23b deregulation derepresses SF-1 and upregulates estrogen signaling in ovarian endometriosis.

J Clin Endocrinol Metab. 2013 Apr;98(4):1575-82. doi: 10.1210/jc.2012-3010. Epub

Shen, Licong| Yang, Shiyuan| Huang, Wei| Xu, Wenming| Wang, Qiushi| Song, Yong| Liu, Ying

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.

CONTEXT: 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. DESIGN: 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. SETTING: The study was conducted at the Department of Gynecology and Obstetrics, West China Second University Hospital of Sichuan University. PATIENTS OR OTHER PARTICIPANTS: We enrolled 23 women with American Fertility Society stage III-IV ovarian endometriosis and 15 disease-free control subjects. INTERVENTIONS: Quantitative real-time RT-PCR, in situ hybridization, cell culture, transfections, and luciferase reporter assays were used in this study. MAIN OUTCOME MEASURES: 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.

Mesh Terms: Adult| Cells, Cultured| Endometriosis/*genetics/metabolism/pathology| Epigenetic Repression/genetics| Estrogens/metabolism/*pharmacology| Female| Gene Expression Regulation/physiology| HEK293 Cells| Humans| MicroRNAs/*genetics/physiology| Ovaria