LncRNA SNHG3 enhances the malignant progress of glioma through silencing KLF2 and p21 (Retracted Article)
LncRNA SNHG3 enhances the malignant progress of glioma through silencing KLF2 and p21 (Retracted Article)
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DOI：
10.1042/bsr20180420
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发表时间：
2018-10-31
影响因子：
4
通讯作者：
Li, Mengni
中科院分区：
文献类型：
--
作者：
Fei, Fan;He, Yongsheng;Li, Mengni
核仁小RNA宿主基因3（SHNG3）是一种新发现的长链非编码RNA，在某些肿瘤中表达异常。然而，SNHG 3对胶质瘤的临床价值和生物学效应的细节仍被覆盖。本研究通过检测SNHG 3在胶质瘤组织和细胞中的表达水平，探讨SNHG 3表达对胶质瘤患者预后的影响。通过功能实验研究SNHG 3对胶质瘤细胞增殖、细胞周期和凋亡等生物学行为的影响。结果表明，SNHG 3在胶质瘤组织和细胞系中的表达明显高于正常组织和细胞系。此外，功能获得或丧失实验表明，SNHG 3的上调促进细胞增殖，加速细胞周期进程，并抑制细胞凋亡。SNHG3通过募集zeste增强子同源物2到KLF 2和p21的启动子，通过表观遗传学抑制KLF 2和p21，促进胶质瘤的恶性进展。SNHG3在胶质瘤中可能是一种癌基因，可作为胶质瘤的潜在预后标志物和治疗靶点。
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.