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.

前列腺癌是最常见的恶性肿瘤之一，也是男性癌症相关死亡的主要原因。越来越多的证据表明，P 元件诱导的 Wimpy (piwi) 相互作用 RNA (piRNA) 在肿瘤进展中起重要作用。很少有研究探讨 piRNA 在前列腺癌进展中的功能机制。在本研究中，我们证明 piR-001773 和 piR-017184 在前列腺癌组织中增加。Protocadherin 9 (PCDH9) 被下调并在前列腺癌细胞中充当肿瘤抑制因子。PCDH9 可以与 PI3K 的调节亚基 p85α 结合。PCa 细胞中 PCDH9 的下调导致 AKT 磷酸化和活性增加。PCDH9 受 piR-001773 和 piR-017184 的转录后调控。体外和体内。此外，piR-001773 和 piR-017184 的下调显着抑制了肿瘤生长。总之，这些结果表明 piR-001773 和 piR-017184 是致癌 RNA，因此可能是前列腺癌的治疗靶点。