NR2F2 regulates bone marrow-derived mesenchymal stem cell-promoted proliferation of Reh cells

被引:12
|
作者
Zhu, Ni [1 ]
Wang, Huafang [1 ]
Wei, Jieping [1 ]
Wang, Binsheng [1 ]
Shan, Wei [1 ]
Lai, Xiaoyu [1 ]
Zhao, Yanmin [1 ]
Yu, Jian [1 ]
Huang, He [1 ]
机构
[1] Zhejiang Univ, Coll Med, Affiliated Hosp 1, Bone Marrow Transplantat Ctr, 79 Qingchun Rd, Hangzhou 310003, Zhejiang, Peoples R China
基金
中国国家自然科学基金;
关键词
NR2F2; mesenchymal stem cells; leukemic cells; proliferation; VEGFA; ACUTE LYMPHOBLASTIC-LEUKEMIA; RECEPTOR COUP-TFII; STROMAL CELLS; DISEASE; CANCER; CYCLE;
D O I
10.3892/mmr.2016.5389
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Bone marrow-derived mesenchymal stem cells (BM-MSCs) are pivotal components of the leukemic microenvironment. BM-MSCs have been previously reported to promote the proliferation of leukemic cells. To further understand the molecular mechanisms of BM-MSC-induced proliferation of leukemic cells, the present study co-cultured acute lymphoblastic leukemia (ALL) Reh cells with BM-MSCs. The current study used methods including shRNA, flow cytometry, MTT, reverse transcription-quantitative polymerase chain reaction, ELISA and western blotting. The data of the present study demonstrated that BM-MSCs promote the proliferation of Reh cells and the NR2F2 mRNA and protein levels were elevated in BM-MSCs following co-culture. Additionally, it was demonstrated that shRNA knockdown of NR2F2 inhibited BM-MSC-induced proliferation of Reh cells. Furthermore, following downregulation of NR2F2, vascular endothelial growth factor A (VEGFA) secretion by BM-MSCs was reduced. The present study demonstrated that NR2F2 mediates BM-MSC-induced proliferation of Reh cells, partially via regulation of VEGFA. Disrupting micro-environmental support by targeting NR2F2 may be a potential therapeutic strategy for ALL.
引用
收藏
页码:1351 / 1356
页数:6
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