MiR–95 promotes osteosarcoma growth by targeting SCNN1A

Abstract

Osteosarcoma (OS) is a common malignant bone tumor, presenting particularly in children and young adults, and accounts for approximately 19% of all malignant bone cancers. Despite advances in OS treatment, long-term prognosis remains poor. miRNAs are non-coding single-stranded RNAs ~22 nucleotides in length. Increasing evidence suggests that numerous miRNAs may play critical roles in tumorigenesis and tumor progression; however, the role of miR-95 in OS has not been examined. In the present study, we investigated the role of miR-95 in OS using in vitro and in vivo models and publicly available expression data. Our findings indicate that abnormal miR-95 expression occurs in OS, according to the Gene Expression Omnibus (GEO) database. The miR-95 inhibitor reduced cell proliferation and promoted apoptosis in OS cell lines as detected by EdU staining, TUNEL staining and flow cytometry. Furthermore, a dual luciferase reporter assay revealed that miR-95 regulates the cell cycle of OS cells and apoptosis by targeting sodium channel epithelial 1α subunit (SCNN1A). Additionally, miR-95 antagomir suppressed the growth of U2OS xenograft tumors in a mouse model. In summary, our results suggest that miR-95 induces OS growth in vitro and in vivo by targeting SCNN1A. Our results help clarify the mechanism underlying the miR-95-mediated effects on OS tumor growth, thus potentially establishing it as a diagnostic target.