文献类型： 外文期刊
作者： Yan, Manli 1 ; Hu, Caihong 2 ; Hu, Qi 3 ; Ma, Heran 4 ; Lei, Changjiang 5 ; Liu, Yamei 6 ;
作者机构： 1.Fifth Hosp Wuhan, Dept Internal Med, Wuhan 430050, Peoples R China
2.China Univ Geosci, Dept Internal Med, Wuhan Hosp, Wuhan 430074, Peoples R China
3.Fifth Hosp Wuhan, Dept Surg, Wuhan 430050, Hubei, Peoples R China
4.Qilu Cell Therapy Technol Co Ltd, Jinan 250100, Peoples R China
5.Fifth Hosp Wuhan, Dept Oncol, Wuhan 430050, Peoples R China
6.Jiangsu Acad Agr Sci, Inst Vet Immunol & Engn, Natl Res Ctr Engn & Technol Vet Biol, Nanjing 210014, Peoples R China
7.Jiangsu Coinnovat Ctr Prevent & Control Important, Yangzhou 225009, Peoples R China
8.GuoTai Taizhou Ctr Technol Innovat Vet Biol, Taizhou 225321, Peoples R China
期刊名称：INTERNATIONAL JOURNAL OF GENOMICS （ 影响因子：2.9； 五年影响因子：2.7 ）
ISSN： 2314-436X
年卷期： 2023 年 2023 卷
页码：
收录情况： SCI
摘要： Background. Recent studies indicate that circular RNAs (circRNAs) have been implicated in the initiation or progression of a wide spectrum of diseases. In the current study, we explored the potential engagement of circ_0008285 in glioma and investigated the downstream regulators. Methods. The detection of circ_0008285 level in glioma specimens and cell lines was conducted by quantitative real-time polymerase chain reaction. The chi-squared test was employed to evaluate the relationship between the circ_0008285 level and the clinical features of glioma patients. The roles of circ_0008285 on the proliferation and apoptosis of glioma cells were studied by knockdown experiment. Meanwhile, the regulatory relationship of circ_0008285, miR-384, and high mobility group protein B1 (HMGB1) was explored in glioma cells, and we explored the effects of circ_0008285/miR-384/HMGB1 pathway on glioma cells. Results. In glioma specimens and cell lines, the expression of circ_0008285 was significantly increased, and a high circ_0008285 level was associated with a larger tumor size and more advanced grading in glioma patients. Furthermore, downregulating circ_0008285 suppressed proliferation and triggered apoptosis of glioma cells, which was associated with a cell cycle arrest at the G1/G0 phase. Mechanism studies indicated that circ_0008285 regulated HMGB1 by sponging miR-384. Functional experiments demonstrated that circ_0008285 promoted the malignant phenotype of glioma cells by miR-384/HMGB1 axis. Conclusion. Our study revealed circ_0008285 as a novel oncogenic factor in glioma through modulating the miR-384/HMGB1 pathway, suggesting that targeting circ_0008285 could serve as a strategy for glioma management.
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