Department of Cardiothoracic Surgery, Huaihe Hospital of Henan University, Kaifeng 475000, China.
Dis Markers. 2017;2017:5314649. doi: 10.1155/2017/5314649. Epub 2017 Sep 25.
Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) was reported to be aberrantly upregulated and promote esophageal squamous cell carcinoma (ESCC) cell progression. Nevertheless, the molecular mechanism of NEAT1 involved in the competing endogenous RNA (ceRNA) regulatory network in ESCC progression remains poorly defined.
The expressions of NEAT1, miR-129, and C-terminal-binding protein 2 (CTBP2) in ESCC cells were examined by qRT-PCR. The effects of NEAT1 knockdown and miR-129 overexpression, or along with CTBP2 upregulation, on ESCC cell viability and invasion were explored by CCK-8 and transwell invasion assays, respectively. Luciferase reporter assay in combination with RIP was performed to confirm the interaction between NEAT1, miR-129, and CTBP2.
NEAT1 and CTBP2 were upregulated and miR-129 was downregulated in ESCC cells. Either NEAT1 knockdown or miR-129 overexpression suppressed ESCC cell viability and invasion. Moreover, NEAT1 functioned as an endogenous sponge to downregulate miR-129 by competitively binding to miR-129, thereby leading to the derepression of CTBP2, a target of miR-129. CTBP2 restoration overturned cell viability and invasion suppression mediated by NEAT1 knockdown or miR-129 overexpression.
LncRNA NEAT1 regulated ESCC cell viability and invasion via the miR-129/CTBP2 axis, contributing to the better understanding of the molecular mechanism of ESCC pathogenesis and progression.
长链非编码 RNA 核斑组装转录本 1（NEAT1）被报道异常上调，并促进食管鳞状细胞癌（ESCC）细胞进展。然而，NEAT1 在 ESCC 进展中的竞争内源性 RNA（ceRNA）调控网络中所涉及的分子机制仍不清楚。
通过 qRT-PCR 检测 ESCC 细胞中 NEAT1、miR-129 和 C 端结合蛋白 2（CTBP2）的表达。通过 CCK-8 和 Transwell 侵袭实验分别研究 NEAT1 敲低和 miR-129 过表达，或与 CTBP2 上调一起对 ESCC 细胞活力和侵袭的影响。通过荧光素酶报告实验结合 RIP 验证 NEAT1、miR-129 和 CTBP2 之间的相互作用。
NEAT1 和 CTBP2 在 ESCC 细胞中上调，miR-129 下调。NEAT1 敲低或 miR-129 过表达均抑制 ESCC 细胞活力和侵袭。此外，NEAT1 通过竞争性结合 miR-129 作为内源性海绵来下调 miR-129，从而导致 miR-129 靶标 CTBP2 的去抑制。CTBP2 的恢复推翻了由 NEAT1 敲低或 miR-129 过表达介导的细胞活力和侵袭抑制。
LncRNA NEAT1 通过 miR-129/CTBP2 轴调节 ESCC 细胞活力和侵袭，有助于更好地理解 ESCC 发病机制和进展的分子机制。
