miR-200b inhibits CD133+ glioma cells by targeting the AKT pathway

被引:16
|
作者
Liu, Aiqun [1 ,2 ]
Yu, Qingyun [2 ]
Peng, Zhongxing [2 ]
Huang, Yeqing [2 ]
Diao, Shengpeng [2 ]
Cheng, Jing [2 ]
Wang, Wentao [3 ]
Hong, Mingfan [2 ]
机构
[1] Jinan Univ, Dept Neurol, Guangzhou 510632, Guangdong, Peoples R China
[2] Guangdong Pharmaceut Univ, Affiliated Hosp 1, Sch Clin Med, Dept Neurol, 16 Jichang Load, Guangzhou 510080, Guangdong, Peoples R China
[3] Guangdong Pharmaceut Univ, Affiliated Hosp 1, Sch Clin Med, Dept Neurosurg, Guangzhou 510080, Guangdong, Peoples R China
基金
美国国家科学基金会;
关键词
glioma; miR-200b; CD133; Akt; PROGNOSTIC-FACTOR; DNA METHYLATION; FEEDBACK LOOP; CANCER CELLS; LUNG-CANCER; CATHEPSIN-B; PROTEIN; CHEMORESISTANCE; MICRORNA-200B; ACTIVATION;
D O I
10.3892/ol.2017.6055
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MicroRNA-200b (miR-200b) is a tumor suppressor in multiple tumor types, including gastric cancer, breast cancer, ovarian cancer and glioma. The biological significance of a known normal and cancer stem cell marker, CD133, remains elusive. The aim of the present study was to identify the function and mechinism of miR-200b in suppressing CD133(+) glioma cells. CD133(+) glioma cells were sorted by flow cytometry. The expression of miR-200b, Ki67, GAP43, GFAP and CD133 were tested by reverse transcription-quantitative polymerase chain reaction. The binding of miR-200b to prominin 1 (PROM1) was certificated by luciferase reporter assay. Cell proliferation was analyzed by bromodeoxyuridine staining. The protein level of CD133, p-AKT, AKT and Notch1 was detected by western blot analysis. Analysis of glioma samples revealed that CD133 expression is negatively associated with miR-200b. PROM1, which is the gene that codes CD133, was certified to be a target of miR-200b. miR-200b expression inhibited the stemness properties and division of the CD133(+) glioma cells. Our results identified a miR-200b/CD133/PI3K/Akt signaling axis, exploring the fundamental role of miR-200b and CD133 in glioma stem cell behavior.
引用
收藏
页码:4701 / 4707
页数:7
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