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miR-183 inhibits the viability, migration and invasion of epithelium on adenomyosis via targeting MMP-9.

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BACKGROUND Adenomyosis refers to a pathological damage resulting from local and diffuse lesions in endometrium, caused by invasive endometrial gland and its mesenchyme. Our study aimed to reveal miR-183's role… Click to show full abstract

BACKGROUND Adenomyosis refers to a pathological damage resulting from local and diffuse lesions in endometrium, caused by invasive endometrial gland and its mesenchyme. Our study aimed to reveal miR-183's role in the development of adenomyosis. METHODS In this context, we separated the epithelium cells of patients with adenomyosis, detected matrix metalloprotein 9 (MMP-9) expression by immunohistochemistry (IHC), and then treated them separately with miR-183 over-expression and miR-183 interference. The effects on epithelium cells funcions with transfections were evaluated by cell viability, migration and invasion assays. Based on that observation, we conducted double luciferase reporting system detection to the screening and the validation of miR-183's target genes. RESULTS It turned out that miR-183 over-expression had a powerful repressive effect on epithelium's viability, migration and invasion; however, the interference in miR-183 contributed a reverse result. Our dual-luciferase assay confirmed that MMP-9 is a target gene of miR-183 in endometrial tissue. Immunohistochemical staining reconfirmed that the fact that MMP-9 was highly expressed in the endometrial tissue of adenomyosis. Importantly, we found that the miR-183 expression in the endometrial tissue of adenomyosis was distinctly lower than normal endometrium. CONCLUSION In general, we are the first to disclose the distinction of miR-183 and MMP-9 expressions in adenomyosis after we elucidated miR-183's role in epithelium's viability, migration and invasion.

Keywords: viability migration; mir 183; adenomyosis; migration invasion

Journal Title: Journal of gynecology obstetrics and human reproduction
Year Published: 2022

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