MicroRNA-509-5p functions as an anti-oncogene in breast cancer via targeting SOD2.

OBJECTIVE:Breast cancer is one of the most common malignant tumors in women worldwide. Considering the poor therapeutic effect of breast cancer, we are supposed to dissect the functioning mode of miR-509-5p on breast cancer cell growth and metastasis, providing therapeutic targets for breast cancer. PATIENTS AND METHODS:Quantitative (qRT-PCR) assay was employed to detect miR-509-5p expression level. CCK8 assay and colony formation assay were incorporated to assess cell viability and proliferation capacities. Cell migration and invasion assay were performed to investigate metastasis capacity of breast cancer cells. Flow cytometry was used to identify cell apoptosis and cell cycle distribution. Protein levels were assessed by Western blotting assay. The target gene was predicted and verified by bioinformatics analysis and luciferase assay. RESULTS:MiR-509-5p was obviously downregulated in breast cancer tissues when compared with pericarcinomatous tissues (n=76). Overexpressed miR-509-5p could attenuate breast cancer cell viability, proliferation, migration and invasion capacities, as well as promote cell apoptosis and induce cell cycle arrest at G0/G1 phase. Superoxide dismutase 2 (SOD2) was chosen as the target gene of miR-509-5p by bioinformatic analysis and Luciferase reporter assay. Moreover, restoration of SOD2 could rescue tumor suppression role of miR-509-5p on breast cancer tumorigenesis. CONCLUSIONS:MiR-509-5p exerted tumor-suppressive effects on breast cancer progression and metastasis via targeting SOD2 in vitro, which provided an innovative and candidate target for diagnose and treatment of breast cancer.

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