Regulatorg Mchanism of MiR-152 on Proliferation, Metastasis and Tumorigenicity of SHI-1 Cells

Abstract

To investigate the regulatory mechanism of miR-152 on proliferation, metastasis and tumorigenesis of human acute monocytic leukemia SHI-1 cells. 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. 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) . 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.