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.

中文翻译：

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长非编码RNA SERTAD2-3通过竞争性结合miR-29c抑制骨肉瘤的增殖和迁移。

背景：骨肉瘤（OS）是一种恶性肿瘤疾病，在儿童和青少年中发病率和死亡率很高。近来，注意力已集中在长非编码RNA（lncRNA）对肿瘤生物学的影响上。在这项研究中，我们确定了lnc-SERTAD2-3在OS发育中的作用。材料和方法：收集60份OS样品和邻近组织，以确定lnc-SERTAD2-3水平与临床病理特征之间的关系。实时定量PCR（qPCR）用于测量基因表达水平。Transwell入侵检测，Cell Counting Kit-8检测和流式细胞仪分别用于测量细胞迁移，生长和凋亡。使用萤光素酶报告基因分析评估了lnc-SERTAD2-3和miR-29c RNA之间的结合位点。结果：与正常组织相比，lnc-SERTAD2-3的表达在OS样品和三种OS细胞系（MG-63，U2OS和Saos-2）中显着下调。lnc-SERTAD2-3表达水平较低的患者预后更差（OS较大，远处转移和复发）。lnc-SERTAD2-3的过表达抑制OS细胞的增殖和迁移，并促进细胞凋亡。而且，我们发现lnc-SERTAD2-3可以通过直接结合抑制miR-29c。此外，miR-29c的重新表达逆转了lnc-SERTAD2-3对OS细胞的作用。结论：总体而言，OS抑制剂lnc-SERTAD2-3通过靶向miR-29c参与了OS增殖和迁移的抑制。lnc-SERTAD2-3表达水平较低的患者预后更差（OS较大，远处转移和复发）。lnc-SERTAD2-3的过表达抑制OS细胞的增殖和迁移，并促进细胞凋亡。而且，我们发现lnc-SERTAD2-3可以通过直接结合抑制miR-29c。此外，miR-29c的重新表达逆转了lnc-SERTAD2-3对OS细胞的作用。结论：总体而言，OS抑制剂lnc-SERTAD2-3通过靶向miR-29c参与了OS增殖和迁移的抑制。lnc-SERTAD2-3表达水平较低的患者预后更差（OS较大，远处转移和复发）。lnc-SERTAD2-3的过表达抑制OS细胞的增殖和迁移，并促进细胞凋亡。而且，我们发现lnc-SERTAD2-3可以通过直接结合抑制miR-29c。此外，miR-29c的重新表达逆转了lnc-SERTAD2-3对OS细胞的作用。结论：总体而言，OS抑制剂lnc-SERTAD2-3通过靶向miR-29c参与了OS增殖和迁移的抑制。此外，miR-29c的重新表达逆转了lnc-SERTAD2-3对OS细胞的作用。结论：总体而言，OS抑制剂lnc-SERTAD2-3通过靶向miR-29c参与了OS增殖和迁移的抑制。此外，miR-29c的重新表达逆转了lnc-SERTAD2-3对OS细胞的作用。结论：总体而言，OS抑制剂lnc-SERTAD2-3通过靶向miR-29c参与了OS增殖和迁移的抑制。