To address these questions we tested the following hypotheses: (i) That Wnt5A protein expression is increased in human prostate cancer (ii) That Wnt/β-catenin signaling should result in increased expression of TCF/LEF target genes such as MMPs and TIMP3 in prostate cancer (iii) Activation of Wnt/Ca2+ signaling in prostate cancer cells should result in an increase in CaMKII enzyme activity causing alterations in cytoskeleton and cell motility. This evidence concerns the gene CAMK2G and prostate carcinoma.