In a previous study we have shown that, in malignant melanoma and prostate cancer, the receptor of the urokinase-plasminogen-activator (uPAR, CD87) is indispensable for supporting a shift from a mesenchymal to an amoeboid movement [13]: uPAR regulates cortical actin contraction/relaxation cycles by interaction with beta1 and beta3 integrins, that in turn connect uPAR to the actin in a RGD-independent fashion. This evidence concerns the gene PLAU and prostate cancer.