Mechanism Study On Proliferation, Invasion And Metastasis Of Breast Cancer Depending On Mir-155 By Adjusting Macc1

Objective: To investigate the mechanism of proliferation, invasion and metastasis that miR-155 affect MCF-7 cell line by adjust the metastasis-associated in colon cancer 1 (MACC1). Methods: Detection the expression of miR-155 in breast cancer tissues and adjacent tissues by RT-PCR, miR-155 inhibitor and miR-155 negative control (NC) that had been constructed were transferred into MCF-7 cell line of breast cancer by Lipofectamine (TM) 2000, the cell viability, proliferation, apoptosis, migration ability, invasion ability were measured successively by MTT assay cloning experiment, propidium iodide (PI) single staining, scratch test, and transwell, RT-PCR was used to detect MACC1 expression in MCF-7 cell line. Luciferase reporter gene analysis (LRGA) verified that MACC1 was a specific downstream target gene of miR-155, and western blot was used to detect the expression of the epithelial cells-mesenchymal transition (EMT) related proteins and MACC1 expression in MCF-7 cell line. Results: The expression of miR-155 in breast cancer was higher than that in adjacent tissues, compared with NC group after miR-155 inhibitor was transferred into MCF-7 cell line by LipofectamineTM2000, the cell viability, clone numbers, and the cell migration ability decreased (P<0.01), the apoptotic cell numbers and the expression of E-cadherin were increased and up-regulated respectively, (P<0.01), the vimentin expression down-regulated. And at the same time the expression of both MACC1 mRNA and protein decreased (P<0.01), LRGA also verified that MACC1 was a specific downstream target gene of miR-155. Conclusion: Interfering with miR-155 gene can significantly inhibit MACC1 expression in MCF-7 cell line and thus inhibit the invasion and metastasis of breast cancer.