Journal
JOURNAL OF BIOLOGICAL CHEMISTRY
Volume 289, Issue 1, Pages 122-132Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M113.502138
Keywords
Cell Invasion; Cell Motility; Dicer; MicroRNA; p63; Cell Scattering; Mutant p53
Categories
Funding
- Cancer Research UK
- AICR (Association For International Cancer Research)
- Breast Cancer Campaign
- Wellcome Trust/The Royal Society
- Medical Research Council
- Breast Cancer Campaign [2011NovPR12] Funding Source: researchfish
- Cancer Research UK [18274] Funding Source: researchfish
- Medical Research Council [MC_UP_1203/3] Funding Source: researchfish
- Wellcome Trust [101242/A/13/Z] Funding Source: researchfish
- Worldwide Cancer Research [11-0626] Funding Source: researchfish
- MRC [MC_UP_1203/3] Funding Source: UKRI
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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 the partial depletion of Dicer, can promote enhanced metastatic potential. We show here that Dicer depletion can promote the invasive behavior of cells that is reflected in enhanced recycling and activation of the growth factor receptors Met and EGF receptor. These responses are also seen in response to the expression of tumor-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.
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