Department of Orthopedics, Weifang People's Hospital, Weifang 261041, Shandong, China.
Department of Oncology, Weifang People's Hospital, Weifang 261041, Shandong, China.
Crit Rev Eukaryot Gene Expr. 2023;33(3):1-11. doi: 10.1615/CritRevEukaryotGeneExpr.2022042373.
Osteosarcoma (OS) is the most representative primary bone tumour in children and teenagers. This study explored the regulatory effects of long noncoding RNA MIR503HG (MIR503HG) on the biological functions of OS cells, and further investigated the potential mechanism of MIR503HG function exertion by analyzing the microRNA-103a-3p (miR-103a-3p) in OS cells and tissues. The expression of MIR503HG was examined using reverse transcription-quantitative PCR. OS cell proliferation was assessed by CCK-8 assay. Transwell assay was used to evaluate the migration and invasion of OS cells. The interaction between MIR503HG and miR-103a-3p was detected using the Dual-luciferase reporter assay. Forty-six paired OS tissues were collected, and the expression and correlation of MIR503HG and miR-103a-3p were evaluated. The expression of MIR503HG were significantly decreased in both OS cells and tissues. Over-expression of MIR503HG inhibited OS cell proliferation, migration and invasion. miR-103a-3p was directly targeted by MIR503HG in OS cells, and mediated the inhibitory effects of MIR503HG on OS cell malignant behaviors. miR-103a-3p expression was upregulated in OS tissues, which was negatively correlated with MIR503HG expression levels. The expression of MIR503HG was associated with OS patients' tumor size, differentiation, distant metastasis and clinical stage. Decreased MIR503HG in OS tissues and cell lines served as a tumor suppressor by inhibiting OS cell malignant behaviors through sponging miR-103a-3p. The findings of this study may provide evidence for the development of novel therapeutic targets of OS.
骨肉瘤（OS）是儿童和青少年中最具代表性的原发性骨肿瘤。本研究探讨了长链非编码 RNA MIR503HG（MIR503HG）对 OS 细胞生物学功能的调节作用，并通过分析 OS 细胞和组织中的 microRNA-103a-3p（miR-103a-3p）进一步探讨了 MIR503HG 功能发挥的潜在机制。采用逆转录定量 PCR 检测 MIR503HG 的表达。通过 CCK-8 测定评估 OS 细胞的增殖。通过 Transwell 测定评估 OS 细胞的迁移和侵袭。采用双荧光素酶报告基因检测法检测 MIR503HG 与 miR-103a-3p 的相互作用。收集 46 对配对的 OS 组织，评估 MIR503HG 和 miR-103a-3p 的表达及相关性。结果显示，MIR503HG 在 OS 细胞和组织中的表达均显著降低。MIR503HG 的过表达抑制了 OS 细胞的增殖、迁移和侵袭。miR-103a-3p 是 OS 细胞中 MIR503HG 的直接靶标，并介导了 MIR503HG 对 OS 细胞恶性行为的抑制作用。miR-103a-3p 在 OS 组织中表达上调，与 MIR503HG 表达水平呈负相关。MIR503HG 的表达与 OS 患者的肿瘤大小、分化、远处转移和临床分期有关。OS 组织和细胞系中 MIR503HG 的表达下调可通过海绵吸附 miR-103a-3p 抑制 OS 细胞恶性行为，发挥肿瘤抑制作用。本研究结果可能为 OS 新的治疗靶点的开发提供依据。
