Lu Hang, Zhang Zhenjun, Lu Yao, Xiu Weiwei, Cui Jinglin
Research Center of Ophthalmology, The First Hospital of Qiqihar, Affiliated Qiqihar Hospital, Southern Medical University, Qiqihar, Heilongjiang Province, People's Republic of China.
Ophthalmology Department, Beiman Hongpeng Hospital of Qiqihar, Qiqihar, Heilongjiang Province, People's Republic of China.
Cancer Manag Res. 2021 Jul 12;13:5587-5597. doi: 10.2147/CMAR.S271326. eCollection 2021.
It is reported that long non-coding RNA nuclear paraspeckle assembly transcript 1 (LncRNA NEAT1) is involved in the occurrence and development of various cancers. However, the detailed biological function and mechanism of LncRNA NEAT1 in retinoblastoma are still unclear. So we will explore the biological function and possible mechanism of LncRNA NEAT1 in retinoblastoma.
Quantitative real-time PCR (qRT-PCR) was used to detect LncRNA NEAT1 in retinoblastoma tissues and cell lines. Cell counting kit 8, Transwell and flow cytometry were applied to explore cell proliferation, invasion and apoptosis. The target miRNAs (miR) of LncRNA NEAT1 and miR and downstream target genes were predicted using Starbase3.0 software and confirmed by double luciferase reporting test and RNA binding protein immunoprecipitation (RIP). Western Blot was applied to explore ROCK1 in cells, and tumor allogeneic experiment was applied to study the role of LncRNA NEAT1 on tumor growth.
It was found that LncRNA NEAT1 was up-regulated in retinoblastoma tissues, cells and serum, and the prognosis of patients with high expression of LNC RNA NEAT 1 was poor. Functional analysis showed that knocking down LncRNA NEAT1 could weaken proliferation and invasion, and accelerate apoptosis. Tumor allogeneic experiment showed that sh-NEAT1 injection can inhibit tumor growth. In addition, LncRNA NEAT1 inhibited proliferation and invasion, and promoted apoptosis through miR-148b-3p/ROCK1 axis.
LncRNA NEAT1 can mediate miR-148b-3p/ROCK1 axis to weaken the proliferation and invasion of retinoblastoma.
据报道，长链非编码RNA核副斑点组装转录本1（LncRNA NEAT1）参与多种癌症的发生发展。然而，LncRNA NEAT1在视网膜母细胞瘤中的详细生物学功能及机制仍不清楚。因此，我们将探讨LncRNA NEAT1在视网膜母细胞瘤中的生物学功能及可能机制。
采用定量实时荧光定量PCR（qRT-PCR）检测视网膜母细胞瘤组织及细胞系中LncRNA NEAT1的表达。应用细胞计数试剂盒8、Transwell实验和流式细胞术检测细胞增殖、侵袭及凋亡情况。使用Starbase3.0软件预测LncRNA NEAT1的靶标微小RNA（miR）以及miR和下游靶基因，并通过双荧光素酶报告基因检测和RNA结合蛋白免疫沉淀（RIP）实验进行验证。采用蛋白质免疫印迹法检测细胞中的ROCK1蛋白表达，通过肿瘤异体移植实验研究LncRNA NEAT1对肿瘤生长的作用。
发现LncRNA NEAT1在视网膜母细胞瘤组织、细胞及血清中表达上调，LNC RNA NEAT1高表达患者的预后较差。功能分析表明，敲低LncRNA NEAT1可减弱细胞增殖和侵袭能力，并加速细胞凋亡。肿瘤异体移植实验表明，注射sh-NEAT1可抑制肿瘤生长。此外，LncRNA NEAT1通过miR-148b-3p/ROCK1轴抑制细胞增殖和侵袭，并促进细胞凋亡。
LncRNA NEAT1可介导miR-148b-3p/ROCK1轴减弱视网膜母细胞瘤的增殖和侵袭能力。
