Inhibition of DDR1 resulted in upregulation of E-cadherin and downregulation of N-cadherin and vimentin protein expression, confirming that DDR1 inhibition decreased cell survival and proliferation of prostate cancer cells by downregulating P-DDR1, P-Pyk2, and P-MKK7 levels, which leads to G1 cell cycle arrest and induced cell death by an increase in the Bax/Bcl-2 ratio, depletion of the mitochondrial membrane potential, and reactive oxygen species creation. Here, DDR1 is linked to prostate carcinoma.