The control and processing of microRNAs (miRs) is critical in the regulation of all cellular responses. Previous studies have suggested that a reduction in the expression of certain miRs, or an overall decrease in miR processing through partial depletion of Dicer, can promote enhanced metastatic potential. We show here that Dicer depletion can promote invasive behavior of cells that is reflected in enhanced recycling and activation of the growth factor receptors Met and EGFR. These responses are also seen in response to the expression of tumour derived mutant p53s, and we show that mutant p53 can down-regulate Dicer expression through both direct inhibition of the TAp63-mediated transcriptional activation of Dicer, and a TAp63 independent control of Dicer protein expression. Our results delineate a clear relationship between mutant p53, TAp63 and Dicer that might contribute to the metastatic function of mutant p53, but interestingly also reveal TAp63 independent functions of mutant p53 in controlling Dicer activity.