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In the present study,we inhibited gene expression of fanconi anemia complementation group-F (FANCF) in breast cancer cells by using RNA interference,and investigated the effects on drug resistance and mechanisms involving the p53 tumor suppressor.FANCF silencing led to increased mitoxantrone (MX) sensitivity and higher intracellular drug concentration in MCF7 cells,as compared to T47D (p53 mutant) cells.The sensitivity to (mitoxantrone) MX was found to be influenced by the p53 functional status in breast cancer cells after FANCF silencing.Furthermore,FANCF silencing in MX-treated MCF7 and T47D breast cancer cells induced overexpression and enhanced function of p53 and subsequent activation of the mitochondrial apoptosis pathway.These effects were more obvious in the MCF7 cells,however,suggesting that FANCF gene silencing could induce drug sensitivity through a mechanism involving a p53-mediated mitochondriai apoptosis pathway in breast cancer cells.In conclusion,we believe that FANCF may be a new target gene for therapeutic reduction or reversal of drug resistance in breast cancer cells,especially in p53 wild-type cancer cells.