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The long noncoding RNA LINC00483 promotes lung adenocarcinoma progression by sponging miR-204-3p
Cellular & Molecular Biology Letters ( IF 9.2 ) Pub Date : 2019-12-16 , DOI: 10.1186/s11658-019-0192-7
Shengzhuang Yang 1 , Tao Liu 1 , Yu Sun 1 , Xiangsen Liang 1
Affiliation  

The expression of the long noncoding RNA LINC00483 is upregulated in lung adenocarcinoma (LUAD). However, its role in the progression of LUAD and the underlying mechanisms remain elusive. The expressions of LINC00483 and miR-204-3p were determined using quantitative real-time PCR. The correlation between the clinicopathological characteristics of LUAD patients and LINC00483 expression was analyzed using Pearson’s χ2 test. A549 and PC-9 cells were transfected with small interfering RNA (siRNA) that specially targeting LINC00483 to assess the impact of its knockdown. Cell proliferation was assessed using the Cell Counting Kit-8 and clone forming assays. Cell migration and cell invasion were evaluated using a transwell assay. The levels of Snail, E-cadherin, N-cadherin and ETS1 proteins were determined via western blotting. The interaction between LINC00483 and miR-204-3p was analyzed using dual-luciferase, fluorescence in situ hybridization and RNA immunoprecipitation. LINC00483 was upregulated in LUAD tissues and cell lines. Higher LINC00483 levels closely correlated to shorter survival times, advanced TNM stage, larger tumor size and positive lymph node metastasis. Cell proliferation, migration and invasion were suppressed after LINC00483 knockdown. LINC00483 mainly localized in the cytoplasm, where it acted as a sponge of miR-204-3p. ETS1 was validated as a downstream target of miR-204-3p and is thus regulated by LINC00483. This study demonstrated that LINC00483 facilitates the proliferation, migration and invasion of LUAD cells by acting as a sponge for miR-204-3p, which in turn regulates ETS1.

中文翻译:


长非编码RNA LINC00483通过海绵miR-204-3p促进肺腺癌进展



长非编码 RNA LINC00483 的表达在肺腺癌 (LUAD) 中上调。然而,其在 LUAD 进展中的作用及其潜在机制仍不清楚。使用定量实时 PCR 测定 LINC00483 和 miR-204-3p 的表达。采用Pearson χ2检验分析LUAD患者临床病理特征与LINC00483表达的相关性。 A549 和 PC-9 细胞用专门针对 LINC00483 的小干扰 RNA (siRNA) 转染,以评估其敲低的影响。使用 Cell Counting Kit-8 和克隆形成测定评估细胞增殖。使用transwell测定评估细胞迁移和细胞侵袭。通过蛋白质印迹法测定 Snail、E-钙粘蛋白、N-钙粘蛋白和 ETS1 蛋白的水平。使用双荧光素酶、荧光原位杂交和 RNA 免疫沉淀分析 LINC00483 和 miR-204-3p 之间的相互作用。 LINC00483 在 LUAD 组织和细胞系中表达上调。较高的 LINC00483 水平与较短的生存时间、较高的 TNM 分期、较大的肿瘤大小和阳性淋巴结转移密切相关。 LINC00483 敲除后,细胞增殖、迁移和侵袭受到抑制。 LINC00483 主要定位于细胞质,充当 miR-204-3p 的海绵。 ETS1 被验证为 miR-204-3p 的下游靶标,因此受到 LINC00483 的调节。这项研究表明,LINC00483 通过充当 miR-204-3p 的海绵,促进 LUAD 细胞的增殖、迁移和侵袭,而 miR-204-3p 反过来又调节 ETS1。
更新日期:2019-12-16
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