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

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. 方法: 将购买的SHI-1细胞系进行miR-152过表达（miR-152 agomir组）或抑制处理（miR-152 antagomir组）并设置阴性对照组（NC组）。应用CCK-8法检测各组细胞活力，划痕愈合实验检测各组细胞迁移能力，Transwell法检测各组细胞侵袭能力，Western blot检测各组细胞Cyclin D1、Caspase-3、MMP-2、TIMP-2、E-cadherin和N-cadherin的表达，Annexin V-FITC/PI双染流式细胞术检测各组细胞凋亡情况，裸鼠成瘤实验检测各组细胞的致瘤性. 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. 结论: miR-152能抑制SHI-1细胞系增殖、转移及致瘤的能力，同时诱导细胞凋亡，其机制可能与miR-152调控MMP-2以及TIMP-2等侵袭转移相关因子有关联.