RESUMO
AIM:To investigate the possible mechanism of microRNA-106a promoting the invasion of human breast cancer MDA-MB-231 cells. METHODS:The efficiencies of transfection with microRNA-106a inhibitor and mi-croRNA-106a mimic by liposome were detected by qPCR. The mRNA and protein expression levels of tissue inhibitor of metalloproteinase 2 (TIMP-2), matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9) in the MDA-MB-231 cells transfected with microRNA-106a mimic were detected by qPCR and Western blot. The effect of microRNA-106a on the invasion ability of MDA-MB-231 cells was measured by Transwell assay. The luciferase reporter assay was used to detect the regulatory effect of microRNA-106a on the TIMP-2 pathway. RESULTS:In the MDA-MB-231 cells, the ex-pression level of microRNA-106a decreased at 48 h after transfection with microRNA-106a inhibitor (P<0.05), and the expression level of microRNA-106a increased at 48 h after transfection with microRNA-106a mimic (P<0.05). The mi-croRNA-106a inhibitor decreased the invasion ability of MDA-MB-231 cells in vitro (P<0.05). The microRNA-106a mim-ic down-regulated the expression of TIMP-2 and up-regulated the expression of MMP2 and MMP9 (P<0.05) in the MDA-MB-231 cells. The microRNA-106a inhibitor enhanced the luciferase activity of the reporter plasmids containing the 3'-un-translated region of TIMP-2 gene (P<0.05), while the microRNA-106a mimic decreased the luciferase activity of the re-porter plasmid (P<0.05). CONCLUSION:High expression of microRNA-106a promotes the invasion ability of breast cancer MDA-MB-231 cells in vitro, which may be related to the inhibition of TIMP-2 pathway. MicroRNA-106a plays an important role in the invasion of breast cancer MDA-MB-231 cells.