These results support our theory that E2F5 and PFTK1 are predominant mediators of miR-1-3p suppression of PCa cell proliferation and cell cycle progression, suggesting that loss of function of miR-1-3p may result in an enhanced expression of E2F5 and PFTK1 and, in turn, the susceptibility of cells to proliferation. Here, E2F5 is linked to posterior cortical atrophy.