In previous studies, downregulation of USP9Y and DDX3Y in lung cancer (LC) tissues was identified, while their function in LC progression remains elusive. In our current work, we intended to elucidate the effect and mechanisms of USP9Y and DDX3Y in LC. Gene downregulation has been confirmed in our LC tissues and cells. The effect of USP9Y or DDX3Y on LC cell malignancies was analyzed by functional assay. Both USP9Y and DDX3Y overexpression showed suppressive impact on LC cell malignancies. USP9Y overexpression has also been demonstrated to inhibit tumorigenesis in vivo. Based on GEPIA database, it was found that there was a positive correlation between the levels of USP9Y and DDX3Y in LC tissues. The mRNA expression of DDX3Y was not affected by USP9Y overexpression, while its protein levels were significantly up-regulated in USP9Y overexpressed LC cells. Moreover, USP9Y interacted with DDX3Y and has been demonstrated to stabilize DDX3Y expression by preventing its degradation via deubiquitination. In conclusion, USP9Y and DDX3Y exerted antioncogenic effects on the cell proliferation potential, cell cycle process, apoptosis, and tumorigenesis of LC. USP9Y binds to DDX3Y to prevent DDX3Y degradation through deubiquitination.

在之前的研究中，我们发现了肺癌（LC）组织中 USP9Y 和 DDX3Y 的下调，但它们在 LC 进展中的功能仍然难以捉摸。在我们目前的工作中，我们旨在阐明 USP9Y 和 DDX3Y 在 LC 中的作用和机制。基因下调已在我们的 LC 组织和细胞中得到证实。通过功能测定分析USP9Y或DDX3Y对LC细胞恶性肿瘤的影响。USP9Y 和 DDX3Y 过表达均显示出对 LC 细胞恶性肿瘤的抑制作用。USP9Y 过表达也被证明可以抑制体内肿瘤发生。基于GEPIA数据库发现LC组织中USP9Y和DDX3Y的水平呈正相关。DDX3Y的mRNA表达不受USP9Y过表达的影响，而其蛋白水平在USP9Y过表达的LC细胞中显着上调。此外，USP9Y 与 DDX3Y 相互作用，并已被证明可以通过去泛素化防止 DDX3Y 降解来稳定 DDX3Y 表达。总之，USP9Y和DDX3Y对LC的细胞增殖潜力、细胞周期过程、细胞凋亡和肿瘤发生具有抗癌作用。USP9Y 与 DDX3Y 结合，防止 DDX3Y 通过去泛素化而降解。