细胞周期蛋白D1
下调和上调
p38丝裂原活化蛋白激酶
细胞生长
癌症研究
免疫印迹
MAPK/ERK通路
基因敲除
化学
分子生物学
信号转导
细胞周期
生物
细胞生物学
细胞
细胞凋亡
生物化学
基因
作者
Ji Ma,Zhenying Gao,Xueni Liu
出处
期刊:PubMed
日期:2021-11-12
卷期号:26 (5): 2084-2089
被引量:3
摘要
To analyze the influence of DDX46 on the proliferative and migratory potentials of glioblastoma (GBM).Differential levels of DDX46 in GBM cases and controls were examined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. By intervening DDX46 in U87 and U251 cells, proliferative and migratory changes were determined by colony formation assay, 5-Ethynyl-2'- deoxyuridine (EdU) assay and Transwell assay, respectively. Protein levels of p-p38, p38, cyclin D1 and MMP7 in GBM cells intervened by DDX46 or the inhibitor of p38 MAPK were detected.DDX46 was upregulated in GBM cases. Knockdown of DDX46 attenuated the proliferative capacity of GBM cells, and its overexpression enhanced the proliferative rate. The migratory capacity of GBM was not affected by DDX46. Overexpression of DDX46 upregulated p-p38 and cyclin D1 in GBM cells. The regulatory effect of DDX46 on GBM proliferation could be partially reversed by the treatment of doramapimod.DDX46 is upregulated in GBM, which strengthens the proliferative capacity of GBM by activating the MAPK-p38 signaling.
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