Jiang Hui, Zheng Haotian, Zhao Xinjie, Xiang Yunzhi, Li Jiahao, Wang Kai, Wang Guanghui, Du Jiajun
Department of Thoracic Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Institute of Oncology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
NPJ Precis Oncol. 2025 Jul 17;9(1):240. doi: 10.1038/s41698-025-01039-9.
RNA-binding proteins (RBPs) play a fundamental role in cellular metabolism, with their disturbance leading to large-scale transcriptomic dysregulation. RBP dysregulation is highly prevalent in human cancers; however, its role in lung adenocarcinoma (LUAD) has not been systematically investigated. To establish a more effective and robust risk model, a machine learning integration program was used to screen hub prognostic RBPs. Our risk model C-index performed extremely well among 103 published signatures. The high-risk group had a lower immune score and worse immunotherapy effects. As one of the members of the RNA helicase family, DDX56 can interact with certain transcription factors, thereby regulating the expression of its downstream targets. DDX56 exerts an anti-apoptotic effect and reduces the sensitivity to carboplatin treatment by promoting Bcl-2 transcription in LUAD cells. Additionally, DDX56 activates NF-kB signaling pathways, which may be related to DDX56-mediated promotion of Bcl-2 transcription, proliferation, migration, and invasion in LUAD patients.
RNA结合蛋白（RBPs）在细胞代谢中发挥着重要作用，其紊乱会导致大规模的转录组失调。RBP失调在人类癌症中极为普遍；然而，其在肺腺癌（LUAD）中的作用尚未得到系统研究。为了建立一个更有效、更稳健的风险模型，使用了一个机器学习整合程序来筛选核心预后RBP。我们的风险模型C指数在103个已发表的特征中表现极为出色。高风险组的免疫评分较低，免疫治疗效果较差。作为RNA解旋酶家族的成员之一，DDX56可以与某些转录因子相互作用，从而调节其下游靶标的表达。DDX56发挥抗凋亡作用，并通过促进LUAD细胞中Bcl-2的转录来降低对卡铂治疗的敏感性。此外，DDX56激活NF-κB信号通路，这可能与DDX56介导的LUAD患者中Bcl-2转录、增殖、迁移和侵袭的促进有关。
