敲减SNORA31抑制胶质瘤干细胞血管生成拟态的作用机制
刘啸白, 王迪, 刘云会中国医科大学附属盛京医院神经外科, 沈阳 110004
收稿日期:
2020-04-11出版日期:
2021-03-30发布日期:
2021-03-20通讯作者:
刘云会E-mail:liuyh_cmuns@163.com作者简介:
刘啸白(1991-),男,讲师,博士.基金资助:
国家自然科学基金(81672511,81872073);中国博士后科学基金(2019M661172);辽宁省自然科学基金(2020-BS-097)关键词: SNORA31, 促红细胞生成素肝细胞受体A2, 血管生成拟态, 胶质瘤干细胞
Abstract: Objective The present study aimed to investigate the expression of SNORA31 in glioma stem cells (GSCs) and the influence of the regulation of erythropoietin-producing hepatocellular receptor A2 (EphA2) on the proliferation,migration,invasion,and vasculogenic mimicry of GSCs. Methods Survival analysis was performed on SNORA31 expression and patient prognosis data obtained from the (chinese gliomagenome atlas,CGGA) database. The expression of SNORA31 in GSCs was detected using qRT-PCR. After SNORA31 knockdown,the expression of EphA2 and phosphorylation of ERK1/2 and PI3K were detected by western blotting. CCK8 and Transwell assays were used to examine alterations in the proliferation,migration,and invasion of GSCs. A matrigel three-dimensional tube formation test was used to detect changes in vasculogenic mimicry. Results Compared with parental cells,the expression of SNORA31 was significantly increased in GSCs (P<0.05). Knockdown of SNORA31 significantly reduced the expression of EphA2,p-ERK1/2/ERK1/2,and p-PI3K/PI3K and inhibited the proliferation,migration,invasion and vasculogenic mimicry of GSCs. Conclusion Knockdown of SNORA31 reduces the phosphorylation of ERK1/2 and PI3K by downregulating EphA2 expression,thereby inhibiting the proliferation,migration,invasion,and vasculogenic mimicry of GSCs.
Key words: SNORA31, erythropoietin-producing hepatocellular receptor A2, vasculogenic mimicry, glioma stem cells
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