Hu Xuanhao, Hong Yang, Shang Chao
Department of Neurobiology, School of Life Science, China Medical University, Shenyang, Liaoning, China.
Department of Neurosurgery, Shengjing Hospital, China Medical University, Shenyang, Liaoning, China.
J Cancer. 2019 Jan 30;10(5):1333-1340. doi: 10.7150/jca.29517. eCollection 2019.
: Human brain glioma is the most malignant primary intracranial tumor, which has poor prognosis and high mortality. Long noncoding RNAs are considered to take part in cellular phenotypes and are emerging as diagnostic and prognostic biomarkers of glioma. This study will research the effects of Small Nucleolar RNA Host Gene 5 (SNHG5) gene on malignant cellular phenotypes in glioma and explore the possible mechanisms. : The expression level of SNHG5 was examined using quantitative Real-time PCR in glioma tissues and cell lines. Loss-of-function experiments of SNHG5 together with Enhanced Cell Counting Kit-8, flow cytometry and cell invasion assay were used to investigate the effects of SNHG5 on malignant cellular phenotypes of glioma cells. Finally, luciferase assay and western blotting were applied to determine the activity of WNT/CTNNB1 signaling pathway. : SNHG5 gene was high-expressed in glioma tissues and cell lines. Knockdown of SNHG5 gene depressed cell proliferation and invasiveness as well as promoted the apoptosis of U251 and U87 cells. In addition, online database analysis showed SNHG5 was closely related to Wnt/CTNNB1 signaling pathway. Knockdown of SNHG5 inactivated Wnt/CTNNB1 signaling pathway, and the activating of Wnt/CTNNB1 signaling pathway partly restored the influences of SNHG5 knockdown on malignant cellular phenotypes of U251 and U87 cells. : SNHG5 gene was high-expressed in glioma, knockdown of SNHG5 inhibits malignant cellular phenotypes of glioma via Wnt/CTNNB1 signaling pathway.
人脑胶质瘤是最恶性的原发性颅内肿瘤,预后差且死亡率高。长链非编码RNA被认为参与细胞表型,正成为胶质瘤的诊断和预后生物标志物。本研究将探讨小核仁RNA宿主基因5(SNHG5)基因对胶质瘤恶性细胞表型的影响,并探索其可能机制。:采用定量实时PCR检测胶质瘤组织和细胞系中SNHG5的表达水平。运用SNHG5功能缺失实验,结合增强型细胞计数试剂盒-8、流式细胞术和细胞侵袭实验,研究SNHG5对胶质瘤细胞恶性细胞表型的影响。最后,采用荧光素酶报告基因检测和蛋白质免疫印迹法检测WNT/CTNNB1信号通路的活性。:SNHG5基因在胶质瘤组织和细胞系中高表达。敲低SNHG5基因可抑制细胞增殖和侵袭能力,并促进U251和U87细胞凋亡。此外,在线数据库分析显示SNHG5与Wnt/CTNNB1信号通路密切相关。敲低SNHG5可使Wnt/CTNNB1信号通路失活,而激活Wnt/CTNNB1信号通路可部分恢复敲低SNHG5对U251和U87细胞恶性细胞表型的影响。:SNHG5基因在胶质瘤中高表达,敲低SNHG5通过Wnt/CTNNB1信号通路抑制胶质瘤的恶性细胞表型。