LncRNA NEAT1 Promotes Gastric Cancer Progression Through miR-17-5p/TGFβR2 Axis Up-Regulated Angiogenesis.
LncRNA NEAT1 Promotes Gastric Cancer Progression Through miR-17-5p/TGFβR2 Axis Up-Regulated Angiogenesis.
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LncRNA NEAT1 通过 miR-17-5p/TGFbetaR2 轴上调血管生成促进胃癌进展
DOI：
10.3389/fcell.2021.705697
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发表时间：
2021
影响因子：
5.5
通讯作者：
Zhang Q
中科院分区：
文献类型：
--
作者：
Xu Y;Li Y;Qiu Y;Sun F;Zhu G;Sun J;Cai G;Lin W;Fu Y;Wu H;Jiang S;Wen Z;Feng F;Luo J;Yang Y;Zhang Q
长链非编码 RNA (lncRNA) 已被证明在胃癌 (GC) 肿瘤发生和进展中发挥关键作用。然而，它们在 GC 中的作用仍有待进一步阐明。采用RT-qPCR和荧光原位杂交（FISH）检测GC组织和细胞系中lncRNA NEAT1的表达。通过基因集富集分析（GSEA）筛选NEAT1可能参与的潜在表型和通路。构建NEAT1沉默的AGS和MGC803细胞并进行一系列功能实验，以研究NEAT1在体外和体内GC血管生成中的作用。 RNA Pull Down 和荧光素酶报告基因检测被用来说明 NEAT1 在 GC 中的功能机制。我们观察到 NEAT1 在大多数 GC 标本和细胞系中表达上调。 NEAT1 高与 GC 患者预后不良相关。体外实验表明，NEAT1通过增强内皮细胞的增殖、迁移和管形成能力来促进GC血管生成。机制研究表明，NEAT1可以竞争性地海绵miR-17-5p，直接靶向TGFβR2。随后，通过上调一系列经典促血管生成因子尤其是 VEGF 来激活 TGFβ/Smad 通路。该研究揭示了 LncRNA NEAT1/miR-17-5p/TGFβR2 轴是 GC 血管生成的一种新机制。破坏该轴可能是 GC 治疗的潜在策略。
Long non-coding RNAs (lncRNAs) have been indicated to play critical roles in gastric cancer (GC) tumorigenesis and progression. However, their roles in GC remain to be further elucidated. RT-qPCR and fluorescence in situ hybridzation (FISH) were conducted to detect the expression of lncRNA NEAT1 in GC tissues and cell lines. Gene Set Enrichment Analysis (GSEA) was performed to screen out potential phenotypes and pathways that NEAT1 may participate in. NEAT1-silenced AGS and MGC803 cells were constructed and a series of functional experiments to investigate the roles of NEAT1 in GC angiogenesis both in vitro and in vivo. RNA pull down and luciferase reporter assays were utilized to illustrate the mechanisms underlying the functions of NEAT1 in GC. We observed that NEAT1 was upregulated in most GC specimens and cell lines. NEAT1 high was correlated with poor prognosis of GC patients. In vitro experiments showed that NEAT1 promoted GC angiogenesis by enhancing proliferation, migration, and tube formation ability of endothelial cells. Mechanism researches revealed that NEAT1 could competitively sponge miR-17-5p which targeted TGFβR2 directly. Subsequently, activate TGFβ/Smad pathway by following with upregulation of a series of classical proangiogenic factors especially VEGF. The study unveiled that the LncRNA NEAT1/miR-17-5p/TGFβR2 axis is a novel mechanism in GC angiogenesis. Disrupting this axis may be a potential strategy for GC treatment.
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影响因子：
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DOI：
10.1186/s13046-020-01718-4
发表时间：
2020-10-08
期刊：
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影响因子：
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作者：
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影响因子：
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作者：
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