lncRNA MAFG-AS1 enhances radioresistance of glioblastoma cells via miR-642a-5p/Notch1 axis

被引:6
|
作者
Zhang, Xi [1 ]
Li, Rui [2 ]
机构
[1] Yaan Peoples Hosp, Dept Oncol, Yaan, Peoples R China
[2] Wenjiang Dist Peoples Hosp, Dept Neurosurg, Chengdu, Peoples R China
关键词
lncRNA MAFG-AS1; miR-642a-5p; Notch1; glioblastoma; radioresistance; CANCER; PROLIFERATION; SUPPRESSION; MECHANISMS; INDUCTION;
D O I
10.55782/ane-2022-030
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
This study was designed to explore the function of lncRNA MAFG-AS1/miR-642a-5p/Notch1 in glioblastoma (GBM) cells under radiation. GBM cells (M059K and M059J) were transfected or/and irradiated. Western blotting was used to detect Notch1 protein and its downstream Hes1 protein. Cell Counting Kit-8 assay and flow cytometry were applied for viability and apoptosis tests, respectively. Luciferase reporter plasmids and Ago2 antibody were used to verify the predicted binding of miR-642a-5p to MAFG-AS1 or Notch1 mRNA. Notch1 and MAFG-AS1 were highly expressed and miR-642a-5p was lowly expressed in radioresistant M059K cells. Knockdown of Notch1 inhibited radioresistance and promoted apoptosis in M059K cells. MAFG-AS1 competed with Notch1 mRNA for binding of miR-642a-5p and therefore promoted the expression of Notch1. Overexpression of miR-642a-5p or silencing of MAFG-AS1 inhibited the radioresistance of M059K cells. Knockdown of Notch1 or overexpression of miR-642a-5p reduced viability and increased apoptosis in irradiated M059J cells overexpressing MAFG-AS1. MAFG-AS1 reduces the radiosensitivity of GBM cells via miR-642a-5p/Notch1 axis.
引用
收藏
页码:315 / 326
页数:12
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