miR-223 regulates malignant biological behavior of acute lymphoblastic leukemia cells through targeting Lmo2 gene and MAPK signal pathway
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Abstract:
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.