Regulatorg Mchanism of MiR-152 on Proliferation, Metastasis and Tumorigenicity of SHI-1 Cells / 中国实验血液学杂志

ABSTRACT

OBJECTIVE@#To investigate the regulatory mechanism of miR-152 on proliferation, metastasis and tumorigenesis of human acute monocytic leukemia SHI-1 cells.@*METHODS@#The purchased SHI-1 cell line was treated with miR-152 over-expression (miR-152 agomir group) or miR-152 inhibition (miR-152 antagomir group), and the negative control (NC) group was set up. The cell proliferation of each group was detected by CCK-8 assay. Scratch healing assay was employed to determine the migration of cells. Transwell assay was used to measure the invasion of cells. The expressions of Cyclin D1, Caspase-3, MMP-2, TIMP-2, E-cadherin and N-cadherin were detected by Western blot. The flow cyronetry with annexin V-FITC/PI double staining was applied to detect the cell apoptosis. The tumorigenesis of cells was examined by tumor formation experiment in nude mice.@*RESULTS@#Compared with the NC group, the cell proliferation, migration and invasion ability in miR-152 agomir group were significantly decreased (P＜0.05), while that in miR-152 antagomir were significantly up-regulated (P＜0.05) . Compared with the NC group, the protein expression of Cyclin D1, MMP-2, N-cadherin were down-regulated in miR-152 agomir group, but the protein expression of Caspase-3, TIMP-2 and E-cadherin were all up-regulated siginificantly. At the same time, the apoptosis were enhanced, but the timorigenicity in nude mice were significantly decreased (all P＜0.05). The protein expression of Cyclin D1, MMP-2, N-cadherin in miR-152 antagomir group, showed high levels but Caspase-3, TIMP-2 and E-cadherin protein showed low levels in comparison with NC group. At the same time, the apoptosis was decreased but the timorigenicity in nude mice was significantly enhanced (all P＜0.05) .@*CONCLUSION@#miR-152 can inhibit the proliferation, metastasis and tumorigenesis of SHI-1 cell line, at the same time induce cell apoptosis, thus providing a theoretical basis for the treatment of acute lymphoblastic leukemia.