Introduction: Prostate cancer is the most common cancer in the UK male population. The disease is characterised by prostate intraepithelial neoplasia followed by metastasis that ultimately results in mortality. Ion channels are implicated in the processes of cell proliferation, migration and survival known to drive cancer progression. Recently, down-regulation of the L-type Ca2+-channel CaV1.2 has been associated with decreased survival of prostate cancer patients1. Our aim was to investigate functional expression of L-type Ca2+-channels in prostate cancer cells. Materials and Methods: A panel of cell lines was used; immortalised normal prostate epithelial cells (RWPE1, PWR1E) and metastatic prostate adenocarcinoma cells (LNCaP, DU145, PC3). Western blot, and RT-PCR were performed to examine protein and gene expression. Cell proliferation WST-1 assays, cell migration scratch-wound healing assays and cell survival clonogenic cell survival assays were performed. Data sets were compared with ANOVA and Newman-Keuls post-hoc test with P<0.05 considered as significant. Results. Protein expression of CaV1.2 and gene expression of the channel subunits, CACNB2 and CACNA2D1 were observed in all cell lines. Gene expression of CACNB2 in LNCaP cells was 6 fold greater (p<0.05, N=3) and CACNA2D1 36 fold greater in PC3 cells (p<0.001, N=3) compared with normals (RWPE1, PWR1E). In prostate cancer DU145 and LNCaP cells, the L-type Ca2+-channel inhibitor verapamil (1µM) significantly decreased proliferation by 16.1±5.2% (p<0.05, N=4) and 27.4±4.9% (p<0.01, N=3) respectively. Nifedipine dose-dependently decreased proliferation in DU145 and LNCaP but this was not significant. PC3 proliferation was unaffected by either inhibitor. In contrast, 0.1µM nifedipine increased proliferation of PWR1E and RWPE1 by 21.1±5.2% (p<0.01, N=4) and 16.2±3.0% (p<0.07, N=3) respectively. L-type Ca2+-channel activators, Bay K8644 and FPL-64176 (0.1-100µM) had no effect on proliferation in the prostate cancer cell lines. In normal PWR1E cells, FPL-64176 (10µM) decreased proliferation by 38.1±5.1% (p<0.01, N=3).Wound healing (migration) of normal cells, RWPE1 and PWR1E was significantly up-regulated in 1µM nifedipine by 11.5±4.1% (p<0.05, N=3) and 27.3±6.3% (p<0.05, N=4) respectively. Verapamil (1μM) also significantly increased PWR1E migration by 26.5±5.4% (p<0.001, N=3). The inhibitors (0.1-100µM) had no effect on migration of DU145 or PC3 cells (p>0.05). In addition, verapamil and nifedipine (0.1-100µM) had no effect on cell survival of the prostate cells examined. Conclusion: These results demonstrate the functional expression of L-type Ca2+-channels in normal and malignant prostate epithelial cells. Inhibition of these channels in normal prostate cells could contribute to development of a malignant phenotype through induction of cell proliferation and migration.