Abstract
The chemo-resistance was one of the major reasons for the treatment failure for breast cancer. Our study aimed to discuss the action of miR-103 derived from BMSC on retarding the chemo-resistance through targeted-regulating TRIAP1 in breast cancer. The cisplatin-resistant breast cancer cells were cultivated and transfected with si-RNA targeting miR-103 followed by analysis of cell invasion, migration and apoptosis by Transwell. MiR-103 target gene was analyzed with bioinformatics method and dual-luciferase reporter assay. TRIAP1 expression was measured by Western Blot. The cell apoptosis was reduced when miR-103 expression was restrained along with enhanced cell proliferation. The co-cultivation with BMSC in vitro could upregulate TRIAP1 expression in breast cancer cells. In cells transfected with si-miR-103, the expression of TRIAP1 was reduced, cell apoptosis was increased and invasion was decreased. In conclusion, the chemo-resistance is induced and the malignant invasion of breast cancer cells is retarded by co-cultivation with mikR-103 derived from BMSC which might be through regulating the expression of TRIAP.
Published Version
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