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首页> 外文期刊>Journal of cellular physiology. >The lncRNASNHG3 accelerates papillary thyroid carcinoma progression via the miR-214-3p/PSMD10 axis
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The lncRNASNHG3 accelerates papillary thyroid carcinoma progression via the miR-214-3p/PSMD10 axis

机译：lncRNASNHG3加速乳头状甲状腺癌进展通过mir - 214 - 3 - p / PSMD10轴

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摘要

Small nucleolar RNA host gene 3 (SNHG3) is a long noncoding RNA (IncRNA), which is known to promote oncogenesis in many cancers but its role in human papillary thyroid carcinoma (PTC) remains poorly understood. We therefore assessed SNHG3 expression in PTC tissues via quantitative reverse transcription polymerase chain reaction. We additionally knocked down SNHG3 in PTC cells using short-hairpin RNAs (shRNAs) to explore its functional roles in PTC. The ability of SNHG3 to bind to specific microRNAs (miRNAs) was predicted using a bioinformatics tool, and this binding was confirmed via dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. We then used a tumor xenograft model to assess the relevance of SNHG3 in vivo. We determined SNHG3 expression to be elevated in PTC tissues relative to controls, with advanced tumor-node-metastasis stage and lymph node metastasis being associated with this expression. Knocking down SNHG3 significantly reduced in vitro PTC cell migration, invasion, proliferation, and colony formation, and it further slowed the growth of tumors in vivo. We found that SNHG3 could bind to miR-214-3p as a competing endogenous RNA (ceRNA) for this miRNA, thereby regulating proteasome 26S subunit non-ATPase 10 (PSMD10) expression, a miR-214-3p target. These results thus indicate that SNHG3 is an oncogenic IncRNA in PTC, acting at least in part via the miR-214-3p/PSMD10 axis.
机译：小核仁的RNA宿主基因3 (SNHG3)是一个长非编码RNA (IncRNA)促进在许多癌症,但它的作用在人类肿瘤形成乳头状甲状腺癌(PTC)仍然不佳理解。通过定量表达PTC组织逆转录聚合酶链反应。我们另外撞倒了SNHG3 PTC细胞探索其使用短发卡rna(成分)在PTC功能的作用。绑定到特定的小分子核糖核酸(microrna)预测使用生物信息学工具,此绑定确认通过dual-luciferase记者和RNA免疫沉淀反应(RIP)化验。异种移植肿瘤模型评估的相关性SNHG3体内。在PTC高架组织相对于控件,先进和tumor-node-metastasis阶段淋巴结转移与此相关表达式。体外PTC细胞迁移,减少入侵,扩散,和集落形成,它进一步的体内肿瘤的生长速度减缓。发现SNHG3可以绑定到mir - 214 - 3 - p竞争这个microrna的内源性RNA(龙头),从而调节26 s蛋白酶体亚基non-ATPase 10 (PSMD10)表达式,mir - 214 - 3 - p目标。PTC的致癌IncRNA,至少在行动通过一部分mir - 214 - 3 - p / PSMD10轴。

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