He Yanli, Nan Haiyan, Yan Linfeng, Ma Tao, Man Minghao, Tian Bo, Guo Shaochun, Zhang Xingye
Department of Radiology, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Oncol Lett. 2021 Feb;21(2):157. doi: 10.3892/ol.2020.12418. Epub 2020 Dec 31.
Glioma is one of the most common and aggressive malignant intracranial tumors worldwide. Recently, non-coding RNAs have been found to play critical roles in the development of glioma. However, the exact mechanisms have not been fully elucidated. In the present study, reverse transcription-quantitative PCR was used to determine the expression level of the long non-coding RNA MIR22HG and microRNA (miR)-9, while western blot analysis was used to detect the protein expression level of CPEB3. The potential binding sites were predicted using the StarBase v2.0 online tool and the hypothesis was verified using a luciferase reporter assay. A Cell Counting Kit-8 assay was used to assess cell viability, while wound healing and Matrigel assays were used to determine the migration and invasion ability of glioma cancer cells. The results showed that MIR22HG expression level was decreased but miR-9 expression level was elevated in glioma tissues and cell lines. Furthermore, MIR22HG was found to sponge miR-9, while CPEB3 was the direct target of miR-9 in the glioma cell line. Functionally, MIR22HG regulated the proliferation, invasion and migration of the glioma cell line by targeting miR-9. CPEB3 may be involved in the progression of the glioma cell line. Taken together, these findings confirmed that MIR22HG suppressed glioma development by inhibiting the miR-9/CPEB3 axis and provides a novel therapeutic strategy for glioma treatment.
胶质瘤是全球最常见且侵袭性最强的恶性颅内肿瘤之一。最近,人们发现非编码RNA在胶质瘤的发展中起关键作用。然而,确切机制尚未完全阐明。在本研究中,采用逆转录定量PCR来测定长链非编码RNA MIR22HG和微小RNA(miR)-9的表达水平,同时利用蛋白质印迹分析来检测CPEB3的蛋白表达水平。使用StarBase v2.0在线工具预测潜在结合位点,并通过荧光素酶报告基因检测验证该假设。采用细胞计数试剂盒-8检测法评估细胞活力,同时利用伤口愈合和基质胶检测法来确定胶质瘤癌细胞的迁移和侵袭能力。结果显示,在胶质瘤组织和细胞系中,MIR22HG表达水平降低但miR-9表达水平升高。此外,发现MIR22HG可吸附miR-9,而在胶质瘤细胞系中CPEB3是miR-9的直接靶点。在功能上,MIR22HG通过靶向miR-9调节胶质瘤细胞系的增殖、侵袭和迁移。CPEB3可能参与胶质瘤细胞系的进展。综上所述,这些发现证实MIR22HG通过抑制miR-9/CPEB3轴抑制胶质瘤发展,并为胶质瘤治疗提供了一种新的治疗策略。