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Down-regulating NEAT1 inhibited the viability and vasculogenic mimicry formation of sinonasal squamous cell carcinoma cells via miR-195-5p/VEGFA axis.
Bioscience Reports ( IF 4 ) Pub Date : 2020-11-04 , DOI: 10.1042/bsr20201373
Honglue Lu 1 , Fei Kang 1
Affiliation  

The role of long non-coding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) in sinonasal squamous cell carcinoma (SNSCC) remained obscure. Target genes and potential binding sites of NEAT1, miR-195-5p and VEGFA were predicted using Starbase and TargetScan, and confirmed by dual-luciferase reporter assay. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expressions of NEAT1, vascular endothelial growth factor A (VEGFA) and miR-195-5p. Pearson's correlation analysis of NEAT1, miR-195-5p and VEGFA was conducted. Cell viability, apoptosis and tube formation capability were assessed by MTT assay, flow cytometry and capillary-like tube formation assay, respectively. Expressions of VEGFA and proteins related to the phosphatidylinositide 3-kinases/Protein Kinase B (PI3K/AKT) pathway were measured by Western blot. In SNSCC tissues and cells, the expressions of NEAT1 and VEGFA were up-regulated while the expression of miR-195-5p was down-regulated, and NEAT1 was negatively correlated with miR-195-5p yet positively correlated with VEGFA. Overexpressed VEGFA promoted the viability and capillary-like tube formation of SNSCC cells yet suppressed their apoptosis, while silencing VEGFA led to the opposite results. MiR-195-5p could bind to NEAT1, and down-regulating miR-195-5p reversed the effects of silencing NEAT1 on the expressions of NEAT1 and miR-195-5p, cell viability, apoptosis and capillary-like tube formation as well as PI3K/AKT pathway activation. VEGFA was the target of miR-195-5p, and overexpressed VEGFA reversed the effects of miR-195-5p. Down-regulating NEAT1 inhibited the viability and vasculogenic mimicry formation of SNSCC cells yet promoted their apoptosis via the miR-195-5p/VEGFA axis, providing a possible therapeutic target for SNSCC treatment.

中文翻译:

下调NEAT1通过miR-195-5p / VEGFA轴抑制了鼻窦鳞状细胞癌细胞的活力和血管生成模拟物的形成。

长期的非编码RNA核富集丰富的转录本1(lncRNA NEAT1)在鼻窦鳞状细胞癌(SNSCC)中的作用仍然不清楚。使用Starbase和TargetScan预测NEAT1,miR-195-5p和VEGFA的靶基因和潜在结合位点,并通过双荧光素酶报告基因测定法进行确认。进行实时定量聚合酶链反应(qRT-PCR),以检测NEAT1,血管内皮生长因子A(VEGFA)和miR-195-5p的表达。进行了NEAT1,miR-195-5p和VEGFA的Pearson相关分析。通过MTT测定,流式细胞术和毛细管样管形成测定分别评估细胞活力,凋亡和管形成能力。通过蛋白质印迹法检测VEGFA和与磷脂酰肌醇3-激酶/蛋白激酶B(PI3K / AKT)途径相关的蛋白的表达。在SNSCC组织和细胞中,NEAT1和VEGFA的表达上调,而miR-195-5p的表达下调,NEAT1与miR-195-5p呈负相关,而与VEGFA呈正相关。过表达的VEGFA促进了SNSCC细胞的活力和毛细血管样形成,但抑制了它们的凋亡,而沉默VEGFA却导致了相反的结果。MiR-195-5p可以与NEAT1结合,而下调miR-195-5p可逆转沉默NEAT1对NEAT1和miR-195-5p表达,细胞活力,细胞凋亡和毛细管样管形成的影响。 PI3K / AKT途径激活。VEGFA是miR-195-5p的靶标,过表达的VEGFA逆转了miR-195-5p的作用。下调NEAT1抑制SNSCC细胞的活力和血管生成模拟物的形成,但通过miR-195-5p / VEGFA轴促进其凋亡,为SNSCC治疗提供了可能的治疗靶点。
更新日期:2020-11-06
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