Subsequently, its artificial overexpression in prostate cancer cell lines promoted apoptosis and cell cycle arrest, inhibiting migration, proliferation, and invasion due to the downregulation of RUNX2 and several downstream targets of RUNX2 (e.g., ANGPTs, MMP11, FAK, osteopontin, osteocalcin, and vimentin) that are linked with prostate cancer bone metastasis. Here, PTK2 is linked to prostate cancer.