Integrins and Mutant p53 on the Road to Metastasis Galina Selivanova, Johanna Ivaska  Cell  Volume 139, Issue 7, Pages 1220-1222 (December 2009) DOI: 10.1016/j.cell.2009.12.016 Copyright © 2009 Elsevier Inc. Terms and Conditions

Figure 1 Mutant p53 and Tumor Metastasis A mutant form of the tumor suppressor protein p53 sequesters p63 (a transcription factor and p53 family member) and blocks its transcriptional activity. This could result in altered expression (red cross) of as yet unknown factors (?) that normally would block the endocytic recycling of the adhesion molecule α5β1-integrin and epidermal growth factor receptor (EGFR). Thus, sequestration of p63 indirectly results in enhanced targeting of α5β1 and EGFR (in a complex with Rab-coupling protein, RCP) back to the plasma membrane. An increase in α5β1-integrin and EGFR at the tumor cell surface boosts the phosphorylation and activation of Akt kinase, which correlates with an increase in the metastatic potential of these cells. Cell 2009 139, 1220-1222DOI: (10.1016/j.cell.2009.12.016) Copyright © 2009 Elsevier Inc. Terms and Conditions