长链非编码 RNA SND1-IT1 通过调控 miR-132-3p/SMAD2 轴促进视网膜母细胞瘤细胞的增殖、侵袭和迁移。
Long non-coding RNA SND1-IT1 accelerates cell proliferation, invasion and migration via regulating miR-132-3p/SMAD2 axis in retinoblastoma.
机构信息
Medical Department of Ophthalmology, Chinese PLA General Hospital, Beijing, China.
Medical Department of Otolaryngology, Head and Neck Surgery, Chinese PLA General Hospital, Beijing, China.
出版信息
Bioengineered. 2021 Dec;12(1):1189-1201. doi: 10.1080/21655979.2021.1909962.
Long noncoding RNAs (lncRNAs) have been identified as prognostic biomarkers and functional regulators in human tumors. In our study, we aim to investigate the roles of lncRNA SND1-IT1 (SND1-IT1) in retinoblastoma (RB). We observed that SND1-IT1 was highly expressed in both RB specimens and cells, and associated with poorer prognosis of RB patients. Functional investigation revealed that downregulation of SND1-IT1 suppressed RB cell proliferation, migration and invasion and restrained RB tumorigenesis in vivo. MiR-132-3p was predicted to interact with SND1-IT1. RT-qPCR and dual-luciferase reporter assays verified the regulation of miR-132-3p by SND1-IT1 in RB cells. In addition, SND1-IT1 enhanced the expression of SMAD2 by sponging miR-132-3p. Rescue experiments revealed that knockdown of miR-132-3p reversed the inhibiting effects of miR-132-3p knockdown on RB cells. Overall, SND1-IT1 can promote the progression of RB cells through miR-132-3p/SMAD2 axis, suggesting that l SND1-IT1 might be a novel biomarker and potential target for RB.
长链非编码 RNA（lncRNA）已被鉴定为人类肿瘤的预后生物标志物和功能调节剂。在我们的研究中，我们旨在研究 lncRNA SND1-IT1（SND1-IT1）在视网膜母细胞瘤（RB）中的作用。我们观察到 SND1-IT1 在 RB 标本和细胞中均高度表达，并与 RB 患者的预后较差相关。功能研究表明，下调 SND1-IT1 抑制 RB 细胞增殖、迁移和侵袭，并抑制体内 RB 肿瘤发生。miR-132-3p 被预测与 SND1-IT1 相互作用。RT-qPCR 和双荧光素酶报告基因检测验证了 SND1-IT1 在 RB 细胞中对 miR-132-3p 的调控作用。此外，SND1-IT1 通过海绵吸附 miR-132-3p 增强了 SMAD2 的表达。挽救实验表明，miR-132-3p 敲低逆转了 miR-132-3p 敲低对 RB 细胞的抑制作用。总的来说，SND1-IT1 可以通过 miR-132-3p/SMAD2 轴促进 RB 细胞的进展，表明 SND1-IT1 可能是 RB 的一种新的生物标志物和潜在靶点。
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