Department of Spinal Surgery, the Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, P.R. China.
Eur Rev Med Pharmacol Sci. 2020 Jul;24(14):7709-7717. doi: 10.26355/eurrev_202007_22274.
Long noncoding RNAs (lncRNAs) play critical roles in osteosarcoma (OS) progression. LncRNA DSCAM-AS1 has been reported to function as a tumor promoter in various cancers. However, the potential mechanism of DSCAM-AS1 in OS remains rarely know.
The expression levels of DSCAM-AS1 and miR-101 were detected by RT-qPCR. The correlation between DSCAM-AS1 and miR-101 expression was analyzed by Pearson's correlation. Kaplan-Meier analysis was used to assess the overall survival rate. Cell viability and invasion were assessed by MTT assay and transwell assays, respectively. A Luciferase reporter assay was used to identify the relationship between DSCAM-AS1 and miR-101.
In the present study, it was demonstrated that DSCAM-AS1 expression was significantly upregulated in OS tissues and cells and high expression of DSCAM-AS1 predicted poor prognosis in OS patients. In addition, the silencing of DSCAM-AS1 suppressed the viability and invasion of OS cells, while DSCAM-AS1 overexpression promoted cell viability and invasion. Furthermore, we found that DSCAM-AS1 inhibited miR-101 expression by direct interaction and DSCAM-AS1 promoted OS progression by sponging miR-101. In addition, miR-101 expression was negatively correlated with DSCAM-AS1 expression. Patients with low miR-101 expression had a shorter overall survival time compared with those with high miR-101 expression.
The present study demonstrated that DSCAM-AS1 accelerated OS cell progression by sponging miR-101, which might provide a new sight in the treatment of OS.
长链非编码 RNA(lncRNA)在骨肉瘤(OS)进展中发挥着关键作用。已有研究报道,lncRNA DSCAM-AS1 在多种癌症中作为肿瘤促进因子发挥作用。然而,DSCAM-AS1 在 OS 中的潜在作用机制仍知之甚少。
通过 RT-qPCR 检测 DSCAM-AS1 和 miR-101 的表达水平。通过 Pearson 相关性分析来分析 DSCAM-AS1 和 miR-101 表达之间的相关性。Kaplan-Meier 分析用于评估总生存率。通过 MTT 测定和 Transwell 测定分别评估细胞活力和侵袭。使用荧光素酶报告基因检测来鉴定 DSCAM-AS1 和 miR-101 之间的关系。
在本研究中,结果表明 DSCAM-AS1 在 OS 组织和细胞中表达显著上调,DSCAM-AS1 高表达预示着 OS 患者预后不良。此外,DSCAM-AS1 的沉默抑制了 OS 细胞的活力和侵袭,而 DSCAM-AS1 的过表达则促进了细胞活力和侵袭。此外,我们发现 DSCAM-AS1 通过直接相互作用抑制 miR-101 的表达,DSCAM-AS1 通过海绵吸附 miR-101 促进 OS 进展。此外,miR-101 的表达与 DSCAM-AS1 的表达呈负相关。与 miR-101 高表达的患者相比,miR-101 低表达的患者总生存时间更短。
本研究表明,DSCAM-AS1 通过海绵吸附 miR-101 加速了 OS 细胞的进展,这可能为 OS 的治疗提供了新的思路。