No abstract

Background: Osteosarcoma (OS) is a malignant tumor disease with high morbidity and mortality in children and adolescents. Recently, attention has been focused on the effects of long noncoding RNAs (lncRNAs) on tumor biology. In this study, we identified the role of lnc-SERTAD2-3 in the development of OS. Materials and Methods: Sixty OS samples and adjacent tissues were collected to determine the relationship between lnc-SERTAD2-3 levels and clinicopathological characteristics. Quantitative real-time PCR (qPCR) was used to measure gene expression levels. A transwell invasion assay, a Cell Counting Kit-8 assay, and flow cytometry were used to measure cell migration, growth, and apoptosis, respectively. The binding site between the lnc-SERTAD2-3 and miR-29c RNAs was evaluated using a luciferase reporter assay. Results: The expression of the lnc-SERTAD2-3 was significantly downregulated in OS samples and three OS cell lines (MG-63, U2OS, and Saos-2) compared to normal tissue. Patients with lower levels of lnc-SERTAD2-3 expression had a more unfavorable prognosis (larger OS size, distant metastasis, and recurrence). Overexpression of lnc-SERTAD2-3 inhibited proliferation and migration, and promoted apoptosis in OS cells. Moreover, we found that lnc-SERTAD2-3 could suppress miR-29c by direct binding. Moreover, reexpression of miR-29c reversed the effect of lnc-SERTAD2-3 on OS cells. Conclusion: Overall, lnc-SERTAD2-3, an OS suppressor, is involved in the inhibition of OS proliferation and migration by targeting miR-29c.