Role and molecular mechanisms of SET mediated pachtaxel resistance in MCF-7/PTX cells

OBJECTIVE: To investigate the resistance mechanisms related to SET in paclitaxel-induced human breast cancer cells. METHODS: The different expressions of SET and ABC transporters between MCF-7/S and paclitaxel resistant MCF-7/PTX cells were identified using Western blot. We adopted siRNA method to knockdown SET in MCF-7/PTX cells and plasmid transfection analysis to up-regulated SET in MCF-7/S cells. The cell viability to paclitaxel was assessed by MTT assay. The cell apoptosis was analyzed by flow cytometry. The levels of ABC transporters were analyzed using Western blot and Real-time PCR, respectively. RESULTS: We found that higher levels of SET and ABC transporters in MCF-7/PTX cells. Knockdown of SET not only significantly sensitized MCF-7/PTX cells to paclitaxel, but also induced cell apoptosis. The levels of the ABC transporters were also reduced. Upregulated SET in MCF-7/S cells expressed resistant to paclitaxel and decreased cell apoptosis. High expression of the SET significantly promotes the mRNA and protein level of ABC transporters. CONCLUSION: The above results demonstrate that SET is associated with paclitaxel resistance in MCF-7/PTX cells. The SET is expected to be one of novel biological targets of overcoming paclitaxel resistant in breast cancer treatment.