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长链非编码 RNA SNHG17 通过调控 miR-23b-3p/ZHX1 轴促进胶质瘤细胞的增殖、迁移和侵袭。

Long non-coding RNA SNHG17 promotes proliferation, migration and invasion of glioma cells by regulating the miR-23b-3p/ZHX1 axis.

机构信息

Department of Neurology, Guangxi Zhuang Autonomous Region Brain Hospital, Liuzhou, Guangxi, China.

Department of Neurosurgery, Guangxi Zhuang Autonomous Region Brain Hospital, Liuzhou, Guangxi, China.

出版信息

J Gene Med. 2020 Nov;22(11):e3247. doi: 10.1002/jgm.3247. Epub 2020 Jul 20.

Abstract

BACKGROUND

Long non-coding RNA (lncRNA) small nucleolar RNA host gene 17 (SNHG17) is a carcinogenic lncRNA in diverse cancers. The expression pattern and mechanisms of SNHG17 in glioma still await verification.

METHODS

Paired glioma samples were enrolled. SNHG17, miR-23b-3p, and zinc-fingers and homeoboxes 1 (ZHX1) mRNA expression were examined by a quantitative real-time polymerase chain reaction (qRT-PCR). SNHG17 short hairpin RNA (shRNA) and miR-23b-3p mimics were transfected into LN229 and U251 cell lines to repress SNHG17 and up-regulate miR-23b-3p expression, respectively. Proliferation, migration and invasion of LN229 and U251 cells were probed by a cell counting kit-8 assay and a Transwell assay. Bioinformatics prediction, dual-luciferase reporter assay, RNA immunoprecipitation assay, qRT-PCR and western blotting were applied to determine the regulatory relationships among SNHG17, miR-23b-3p and ZHX1.

RESULTS

SNHG17 expression was markedly raised in glioma tissues, which was positively correlated with ZHX1 expression and negatively associated with the expression of miR-23b-3p. After transfection of SNHG17 shRNAs into glioma cells, the proliferation, migration and invasion of cancer cells was markedly restrained. miR-23b-3p mimics the function of SHNG17 knockdown. Furthermore, miR-23b-3p was shown to be negatively modulated by SNHG17, and ZHX1 was identified as a target of miR-23b-3p.

CONCLUSIONS

SNHG17 is a "competing endogenous RNA" with respect to modulating ZHX1 expression by adsorbing miR-23b-3p and thereby promoting glioma progression.

摘要

背景

长链非编码 RNA(lncRNA)小核仁 RNA 宿主基因 17(SNHG17)是多种癌症中的致癌 lncRNA。SNHG17 在神经胶质瘤中的表达模式和机制仍有待验证。

方法

纳入配对的神经胶质瘤样本。通过实时定量聚合酶链反应(qRT-PCR)检测 SNHG17、miR-23b-3p 和锌指和同源盒 1(ZHX1)mRNA 的表达。将 SNHG17 短发夹 RNA(shRNA)和 miR-23b-3p 模拟物转染至 LN229 和 U251 细胞系中,分别抑制 SNHG17 并上调 miR-23b-3p 的表达。通过细胞计数试剂盒-8 检测和 Transwell 检测来探测 LN229 和 U251 细胞的增殖、迁移和侵袭。应用生物信息学预测、双荧光素酶报告基因检测、RNA 免疫沉淀检测、qRT-PCR 和 Western blot 来确定 SNHG17、miR-23b-3p 和 ZHX1 之间的调控关系。

结果

SNHG17 在神经胶质瘤组织中的表达明显升高,与 ZHX1 的表达呈正相关,与 miR-23b-3p 的表达呈负相关。转染 SNHG17 shRNA 后,癌细胞的增殖、迁移和侵袭明显受到抑制。miR-23b-3p 模拟物可模拟 SHNG17 敲低的功能。此外,miR-23b-3p 受 SNHG17 负调控,ZHX1 是 miR-23b-3p 的靶基因。

结论

SNHG17 是一种“竞争内源性 RNA”,通过吸附 miR-23b-3p 调节 ZHX1 的表达,从而促进神经胶质瘤的进展。

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