目的： 探讨miR-223调控急性淋巴细胞白血病（acute lymphoblastic leukemia，ALL）E6-1细胞的增殖和体内成瘤能力及其作用机制。 方法： 应用实时荧光定量PCR检测miR-223在不同ALL细胞株中的表达水平，免疫荧光染色法检测携带miR-223mimic慢病毒感染E6-1细胞株的感染效率，双荧光素酶实验检测miR-223和Lmo2的相互结合关系，MTT增殖实验和克隆形成实验检测过表达miR-223对E6-1细胞株增殖和克隆形成能力的影响。裸鼠体内成瘤实验检测miR-223过表达对E6-1细胞成瘤能力的影响。Western blotting检测miR-223对MAPK信号通路相关蛋白表达的影响。 结果： miR-223在E6-1细胞株中表达水平相对较低（P<0.05），双荧光素酶实验证实miR-223可以直接靶向结合Lmo2的3’UTR区序列。过表达miR-223后： （1）抑制E6-1细胞的增殖能力（0.16±0.02 vs 1.15±0.21，P<0.05）； （2）抑制E6-1细胞的裸鼠体内成瘤能力[ （0.56±0.08）vs（1.69±0.22）g，P<0.05]； （3）调控MAPK信号通路的活性。 结论： miR-223可靶向作用Lmo2通过MAPK信号通路调控ALL细胞的增殖、克隆形成和体内成瘤能力。

Objective: To investigate the effect and mechanism of miR-223 regulating the proliferation and in vivo tumorigenesis of acute lymphoblastic leukemia (ALL) E6-1 cells. Methods: The expression of miR-223 in different ALL cell lines was detected by Real-time fluorescence quantitative PCR. Immunofluorescence was used to detect the transfection efficiency of miR-223mimic-lenitvirus transfected E6-1 cell line. Double luciferase assay was used to detect the binding between miR-223 and Lmo2. MTT assay and clone formation assay were used to detect the ef-fect of miR-223 on the proliferation and clone formation ability of E6-1 cell line. The effect of miR-223 expression on the tumorigenic ability of E6-1 cells was detected by xenograft formation in nude mice. Western blotting was used to detect the effect of miR-223 on the expressions of MAPK signal pathway related proteins. Results: The ex-pression level of miR-223 in E6-1 cell line was relatively low (P<0.05). Double luciferase assay confirmed that miR-223 could directly target the 3’UTR of Lmo2. Overexpression of miR-223 inhibited the proliferation (0.16±0.02 vs 1.15±0.21，P<0.05) and tumorigenesis ([0.56±0.08]g vs [1.69±0.22]g，P<0.05) of E6-1 cells and regulated the ac-tivity of MAPK signal pathway. Conclusion: miR-223 can regulate the proliferation, clone formation and in vivo tu-morigenesis ofALL cells through targeting Lmo2 and MAPK signal pathway.