Epsins have an important role in mediating
clathrin-mediated endocytosis of ubiquitinated
cell surface receptors. The potential role for epsins in
tumorigenesis and
cancer metastasis by regulating intracellular signaling pathways has largely not been explored. Epsins are reportedly upregulated in several types of
cancer including human skin, lung, and canine
mammary cancers. However, whether their expression is elevated in
prostate cancer is unknown. In this study, we investigated the potential role of epsins in prostate
tumorigenesis using the wild type or
epsin-deficient human
prostate cancer cells, LNCaP, in a human xenograft model, and the spontaneous TRAMP mouse model in wild type or
epsin-deficient background. Here, we reported that the expression of epsins 1 and 2 is upregulated in both human and mouse
prostate cancer cells and cancerous tissues. Consistent with upregulation of epsins in prostate
tumors, we discovered that depletion of epsins impaired
tumor growth in both the human LNCaP xenograft and the TRAMP mouse prostate. Furthermore,
epsin depletion significantly prolonged survival in the TRAMP mouse model. In summary, our findings suggest that epsins may act as oncogenic
proteins to promote prostate
tumorigenesis and that depletion or inhibition of epsins may provide a novel therapeutic target for future
prostate cancer therapies.