Prostate cancer is one of the most common malignancies and the major cause of cancer-related death in men. Increasing evidence has revealed that P-element-induced wimpy (piwi)-interacting RNAs (piRNAs) play an important role in tumor progression. Few studies have been explored the functional mechanism of piRNAs in prostate cancer progression. In the present study, we demonstrated that piR-001773 and piR-017184 were increased in prostate cancer tissues. Protocadherin 9 (PCDH9) was downregulated and acted as a tumor suppressor in prostate cancer cells. PCDH9 could bind to p85α, the regulatory subunit of PI3K. The downregulation of PCDH9 in PCa cells resulted in an increase in AKT phosphorylation and activity. PCDH9 was posttranscriptionally regulated by piR-001773 and piR-017184. The upregulation of piR-001773 and piR-017184 promoted tumor growth both in vitro and in vivo. In addition, the downregulation of piR-001773 and piR-017184 markedly inhibited tumor growth. In conclusion, these results indicated that piR-001773 and piR-017184 are oncogenic RNAs and thus might be therapeutic targets in prostate cancer.