Department of Hematology, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, China.
Department of Internal Medicine, Zhejiang Provincial People's Hospital, People's Hospital of Hangzhou Medical College, Hangzhou, China.
J Biol Regul Homeost Agents. 2018 Nov-Dec;32(6):1467-1471.
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 T-ALL cell proliferation, survival and invasion using gain and loss of function approaches. Human Jurkat cells, a widely used 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 T-ALL by negatively regulating the NOTCH1 signaling pathway.
微小 RNA-200b（miR-200b）在人类肺癌中作为致癌调节剂发挥作用。然而，miR-200b 对 T 细胞急性淋巴细胞白血病（T-ALL）的发展和进展的影响在很大程度上仍然未知。在这项研究中，我们使用功能获得和功能丧失方法评估了 miR-200b 在 T-ALL 细胞增殖、存活和侵袭中的作用。人 Jurkat 细胞是一种广泛使用的 T-ALL 细胞模型，用 miR-200b 模拟物或 miR-200b 抑制剂转染。与对照 miRNA 处理的细胞相比，miR-200b 模拟物可显著抑制 Jurkat 细胞增殖和侵袭，同时显著刺激细胞凋亡。相反，用抗 miR200 处理的 Jurkat 细胞显示出诱导细胞生长和侵袭，但抑制细胞凋亡。这种效应伴随着 NOTCH1 表达的相应改变，表明 NOTCH1 可能是 miR-200b 在 Jurkat 细胞中发挥作用的靶基因。总之，我们的研究结果表明，miR-200b 通过负调控 NOTCH1 信号通路可能成为 T-ALL 的潜在治疗靶点。
