In this study, we founded that API treatment of PCa cells caused a decrease in SPOCK1 expression subsequently leading to inhibition of the invasive abilities and EMT-related markers (Snail, Slug and vimentin), while overexpression of SPOCK1 could reverse the API-mediated inhibitory effects, suggesting that SPOCK1 inhibition by API may be the main cause for the API-mediated suppression of Snail family-induced cell motility in PCa. The gene discussed is SNAI1; the disease is posterior cortical atrophy.