miR-532-3p is a widely documented microRNA (miRNA) involved in multifaceted processes of cancer tumorigenesis and metastasis. However, the clinical significance and biological functions of miR-532-3p in bone metastasis of prostate cancer (PCa) remain largely unknown. Herein, we report that miR-532-3p was downregulated in PCa tissues with bone metastasis, and downexpression of miR-532-3p was significantly associated with Gleason grade and serum prostate-specific antigen (PSA) levels and predicted poor bone metastasis-free survival in PCa patients. Upregulating miR-532-3p inhibited invasion and migration abilities of PCa cells in vitro, while silencing miR-532-3p yielded an opposite effect on invasion and migration abilities of PCa cells. Importantly, upregulating miR-532-3p repressed bone metastasis of PCa cells in vivo. Our results further demonstrated that overexpression of miR-532-3p inhibited activation of nuclear facto κB (NF-κB) signaling via simultaneously targeting tumor necrosis factor receptor-associated factor 1 (TRAF1), TRAF2, and TRAF4, which further promoted invasion, migration, and bone metastasis of PCa cells. Therefore, our findings reveal a novel mechanism contributing to the sustained activity of NF-κB signaling underlying the bone metastasis of PCa.

miR-532-3p是广泛报道的microRNA（miRNA），参与癌症肿瘤发生和转移的多方面过程。然而，miR-532-3p在前列腺癌（PCa）骨转移中的临床意义和生物学功能仍然未知。在此，我们报道miR-532-3p在具有骨转移的PCa组织中下调，而miR-532-3p的下表达与Gleason分级和血清前列腺特异性抗原（PSA）水平显着相关，并预测无不良骨转移PCa患者的生存率。上调miR-532-3p抑制PCa细胞的体外侵袭和迁移能力，而沉默miR-532-3p对PCa细胞的侵袭和迁移能力产生相反的影响。重要的是，在体内miRNA-532-3p的上调抑制了PCa细胞的骨转移。我们的结果进一步证明，miR-532-3p的过表达通过同时靶向肿瘤坏死因子受体相关因子1（TRAF1，TRAF2和TRAF4）抑制核因子κB（NF-κB）信号的激活，从而进一步促进了侵袭，迁移和PCa细胞的骨转移。因此，我们的发现揭示了一种新的机制，该机制有助于PCa骨转移背后的NF-κB信号的持续活性。