miR-200b PROMOTES CELL PROLIFERATION AND INVASION IN T-CELL ACUTE LYMPHOBLASTIC LEUKEMIA THROUGH NOTCH1

被引:1
|
作者
Ning, F. [1 ]
Zhou, Q. [2 ]
Chen, X. [3 ]
机构
[1] Hangzhou Med Coll, Peoples Hosp, Zhejiang Prov Peoples Hosp, Dept Hematol, 158 Shangtang Rd, Hangzhou 310000, Zhejiang, Peoples R China
[2] Hangzhou Med Coll, Peoples Hosp, Zhejiang Prov Peoples Hosp, Dept Internal Med, Hangzhou, Zhejiang, Peoples R China
[3] Hangzhou Med Coll, Peoples Hosp, Zhejiang Prov Peoples Hosp, Dept Resp Med, Hangzhou, Zhejiang, Peoples R China
关键词
miR-200b; NOTCH1; T-ALL; microRNA; SIGNALING PATHWAY; PROGRESSION; EXPRESSION;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
MicroRNA-200b (miR-200b) functions as an oncogenic regulator in human lung cancer. However, the effect of miRNA-200b on the development and progression of T-Cell acute lymphoblastic leukemia (T-ALL) remains largely unknown. In this study, we evaluated the impact of miR-200b in TALL cell proliferation, survival and invasion using gain and loss of function approaches. Human Jurkat cells, a widely used in-vitro T-ALL cell model, were transfected with miR-200b mimic or miR-200b inhibitor. miR-200b mimics substantially inhibited Jurkat cell proliferation and invasion while significantly stimulating cell apoptosis compared to the control miRNA-treated cells. In contrast, Jurkat cells treated with anti-miR200 demonstrated induction of cell growth and invasion but repression of cell apoptosis. Such effect was accompanied by the corresponding alteration in NOTCH1 expression, suggesting that NOTCH1 might be the target gene for miR-200b function in Jurkat cells. In summary, our findings demonstrate that miR-200b may serve as a potential therapeutic target for TALL by negatively regulating the NOTCH1 signaling pathway.
引用
收藏
页码:1467 / 1471
页数:5
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