The ability of a cell to escape the constraints of the local environment and colonise distal sites is strictly dependant on acquiring the means to circumvent normal cell-extracellular matrix regulation. β1 integrin, a major extracellular receptor, regulates the response of both normal and cancer cells to their local environment. Although mis-localised in prostate cancer, the role β1 integrin plays in prostate development and carcinogenesis remains unknown. To investigate the role of integrins and integrin signalling in prostate development and cancer, we conditionally deleted β1 integrin and two downstream signaling molecules, Ilk and Fak from the prostate. In addition to examination of normal prostate development, we also assessed the effects of β1 integrin, Ilk and Fak deletion on tumour progression in the TRAMP and PTEN prostate carcinogenesis models. Deletion of β1 integrin following castration and subsequent androgen supplementation resulted in an expansion of the p63-positive basal cell population and decreased differentiation. Deletion of β1 integrin also resulted in dramatic enlargement of the seminal vesicles perturbing differentiation through Ilk and the Akt pathway. In contrast to other systems such as breast, β1 integrin deletion in TRAMP mice decreased animal survival, decreased retention of normal prostate morphology, increased the percentage of tissue with poorly-differentiated carcinoma, and increased cell proliferation. Conditional deletion of the downstream integrin effectors Ilk and Fak, reviled that deletion of Fak had the opposite effects, decreasing cancer cell proliferation and enhancing survival in the TRAMP prostate cancer model. This study demonstrates that β1 integrin regulates several aspects of normal prostate development and in contrast to its role in several other tissues, its loss is associated with increased rates of prostate tumour progression. These data also point to novel roles for β1 integrin and Fak as potential therapeutic targets in prostate cancer.