[No authors listed]
Many reports suggest that the discovery of microRNAs (miRNAs) might provide a novel therapeutical target for many diseases, even of human cancers; however, there are no reports on the role of miR-597 in human cancers. In the present study, by detecting mRNA expression with qRT-PCR, compared with the adjacent normal tissues we found that miR-597 was significantly downregulated in breast cancer tissues. By using the MTT assay, the cell wound-healing assay and the cell invasion assay, we demonstrated that miR-597 mimics were able to suppress breast cancer cell proliferation, migration and invasion. Additionally, with flow cytometry, we found that mir-597 influenced the growth of breast cancer cells through regulating the G1-S phase transition. Furthermore, we identified one binding site for miR-597 at the 3'UTR of the FOSL2 gene, using bioinformatics methods and the luciferase reporter assay, it was confirmed that FOSL2 was a direct target of miR-597. Moreover, overexpression of FOSL2 in MDA-MBâ231 and SK-BR-3 cells can block the vast majority of the miR-597 roles, suggesting that miR-597 acts as a tumor suppressor in breast cancer cells by the downregulation of FOSL2. Additionally, we also found a negative correlation between the expression of FOSL2 and miR-597 in the tumor samples. This new regulatory mechanism in breast cancer may provide another method for diagnosis and therapy.
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