[No authors listed]
OBJECTIVE:To analyze the functioning mode of miR-645 on breast cancer cell metastasis and provide therapeutic targets for breast cancer. MATERIALS AND METHODS:Quantitative (qRT-PCR) assay was employed to detect miR-645 expression level. Wound healing assay and transwell assay were performed to investigate metastasis capacity of breast cancer cells. Protein levels were assessed by Western blotting assay. The target gene was predicted and verified by bioinformatics analysis and luciferase assay. RESULTS:MiR-645 was upregulated in breast cancer tissues when compared with pericarcinous tissues (n=60). Downregulated miR-645 could attenuate breast cancer cell migration and invasion capacities, as well as inhibit the process of epithelial-mesenchymal transition (EMT). DCDC2 was chosen as the target gene of miR-645 by bioinformatic analysis and Luciferase reporter assay. Moreover, the silence of DCDC2 could rescue tumor suppression role of downregulated miR-645 on breast cancer metastasis. CONCLUSIONS:Knockdown of miR-645 exerted tumor-suppressive effects on breast cancer metastasis via targeting DCDC2 in vitro, which provided an innovative and candidate target for diagnose and treatment of breast cancer.
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