MicroRNA-34a induces transdifferentiation of glioma stem cells into vascular endothelial cells by targeting Notch pathway

被引:21
|
作者
Jin, Zaishun [1 ]
Zhan, Tao [2 ]
Tao, Jing [3 ]
Xu, Biao [4 ]
Zheng, Huizhe [2 ]
Cheng, Yongxia [2 ]
Yan, Bin [2 ]
Wang, Hongwei [2 ]
Lu, Guoqiang [5 ]
Lin, Ying [6 ]
Guo, Sufen [1 ,2 ]
机构
[1] Mudanjiang Med Univ, Key Lab Canc Prevent & Treatment Heilongjiang Pro, Mudanjiang, Peoples R China
[2] Mudanjiang Med Univ, Dept Pathol, Mudanjiang, Peoples R China
[3] Mudanjiang Med Univ, Dept Rehabil Med, Hongqi Hosp, Mudanjiang, Peoples R China
[4] Mudanjiang Med Univ, Dept Cardiol, Hongqi Hosp, Mudanjiang, Peoples R China
[5] Mudanjiang Med Univ, Dept Sci Res, Mudanjiang, Peoples R China
[6] Mudanjiang Med Univ, Dept Thorac Surg, Hongqi Hosp, Mudanjiang, Peoples R China
关键词
delta like 1; glioma stem cells; microRNA; 34a; Notch; 1; vascular endothelial cells; GLIOBLASTOMA-MULTIFORME; TUMOR ANGIOGENESIS; IN-VITRO; MECHANISMS; SUPPRESSOR; BIOMARKER; GROWTH; NICHE;
D O I
10.1080/09168451.2017.1364965
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The function of microRNA-34a (miR-34a) in transdifferentiation of glioma stem cells (GSCs) into vascular endothelial cells (VECs) was explored by focusing on Notch ligand Delta-like 1 (Dll1). MiR-34a mimics was transfected into CD133 + glioma cell U251. The angiogenesis feature of miR-34a transfected U251 cells was investigated and the expressions of CD31, CD34, Vwf, Notch 1, and Dll1 were quantified. Length of branching vessel-like structures in the miR-34a transfected U251 cells was significantly higher than control cells. The VEC feature of miR-34a overexpressed U251 cells was further confirmed by the expressions of CD31, CD34, and vWF. Transfection of miR-34a decreased the expression of Notch 1 and Dll1. Furthermore, the miR-34a overexpression-enhanced tube formation of GSCs was suppressed when the decreased expression of Dll1 was restored. The current study highlighted the potential of miR-34a as an inducer in GSCs' transdifferentiation into VECs by targeting Dll1.
引用
收藏
页码:1899 / 1907
页数:9
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