长链非编码 RNA SNHG3 通过沉默 KLF2 和 p21 促进脑胶质瘤的恶性进展。

LncRNA SNHG3 enhances the malignant progress of glioma through silencing KLF2 and p21.

机构信息

Department of Neurosurgery, Hospital of The University of Electronic Science and Technology of China and Sichuan Provincial People's Hospital, No.32 West Second Section First Ring Road, Chengdu 610072, Sichuan, China.

Department of Neurosurgery, Graduate School of Zunyi Medical University, Zunyi 563003, Guizhou, China.

出版信息

Biosci Rep. 2018 Sep 7;38(5). doi: 10.1042/BSR20180420. Print 2018 Oct 31.

As a newly discovered long non-coding RNA, small nucleolar RNA host gene 3 (SHNG3) has been reported to be dysregulated in certain cancers. Nevertheless, the details about clinical values and biological effects of SNHG3 on glioma are still covered. In this paper, we determined the expression level of SNHG3 in glioma tissues and cells and evaluated the effect of SNHG3 expression on the prognosis of glioma patients. The functional assays were applied to define the effects of SNHG3 on the biological behaviors in glioma including cell proliferation, cell cycle, and apoptosis. It was revealed that SNHG3 was much more enriched in glioma tissues and cell lines than in normal ones. Furthermore, gain- or loss-of-function experiments indicated that the up-regulation of SNHG3 promoted cell proliferation, accelerate cell cycle progress, and repressed cell apoptosis. The mechanistic assays disclosed that SNHG3 facilitated the malignant progression of glioma through epigenetically repressing KLF2 and p21 via recruiting enhancer of zeste homolog 2 to the promoter of KLF2 and p21. Generally, it was exposed that SNHG3 might function as an oncogene in glioma and could be explored as a potential prognostic biomarker and therapeutic target for glioma.

作为一种新发现的长非编码 RNA，小核仁 RNA 宿主基因 3（SHNG3）在某些癌症中被报道存在失调。然而，关于 SNHG3 对神经胶质瘤的临床价值和生物学效应的细节仍不清楚。在本文中，我们测定了 SNHG3 在神经胶质瘤组织和细胞中的表达水平，并评估了 SNHG3 表达对神经胶质瘤患者预后的影响。功能分析用于确定 SNHG3 对神经胶质瘤生物学行为的影响，包括细胞增殖、细胞周期和细胞凋亡。结果表明，SNHG3 在神经胶质瘤组织和细胞系中的含量明显高于正常组织和细胞系。此外，功能获得和功能丧失实验表明，SNHG3 的上调促进了细胞增殖，加速了细胞周期进程，抑制了细胞凋亡。机制分析表明，SNHG3 通过招募增强子结合蛋白 2（EZH2）到 KLF2 和 p21 的启动子上来抑制 KLF2 和 p21 的表达，从而促进神经胶质瘤的恶性进展。总的来说，SNHG3 可能在神经胶质瘤中发挥癌基因的作用，并可作为神经胶质瘤潜在的预后标志物和治疗靶点。