Recent studies have shown that NOP2, a nucleolar protein, is up-regulated in various cancers, suggesting a potential link to tumor aggressiveness and unfavorable outcomes. This study examines NOP2's role in lung adenocarcinoma (LUAD), a context where its implications remain unclear. Utilizing bioinformatics, we assessed 513 LUAD and 59 normal tissue samples from The Cancer Genome Atlas (TCGA) to explore NOP2's diagnostic and prognostic significance in LUAD. Additionally, in vitro experiments compared NOP2 expression between Beas-2b and A549 cells. Advanced databases and analytical tools, including LINKEDOMICS, STRING, and TISIDB, were employed to further elucidate NOP2's association with LUAD. Our findings indicate a significantly higher expression of NOP2 mRNA and protein in A549 cells compared to Beas-2b cells (P < 0.001). In LUAD, elevated NOP2 levels were linked to decreased Overall Survival (OS) and advanced clinical stages. Univariate Cox analysis revealed that high NOP2 expression correlated with poorer OS in LUAD (P < 0.01), a finding independently supported by multivariate Cox analysis (P < 0.05). The relationship between NOP2 expression and LUAD risk was presented via a Nomogram. Additionally, Gene Set Enrichment Analysis (GSEA) identified seven NOP2-related signaling pathways. A focal point of our research was the interplay between NOP2 and tumor-immune interactions. Notably, a negative correlation was observed between NOP2 expression and the immune infiltration levels of macrophages, neutrophils, mast cells, Natural Killer (NK) cells, and CD8 + T cells in LUAD. Moreover, the expression of NOP2 was related to the sensitivity of various chemotherapeutic drugs. In vitro, we found that downregulating NOP2 can decrease the proliferation, migration and invasion of A549 cells. Furthermore, NOP2 can regulate Caspase3-mediated apoptosis. Collectively, particularly regarding prognosis, immune infiltration and vitro experiments, these findings suggest NOP2's potential of serving as a poor-prognostic biomarker for LUAD and aggravating the malignancy of lung adenocarcinoma cells.

最近的研究表明，NOP2（一种核仁蛋白）在多种癌症中表达上调，这表明它与肿瘤侵袭性和不良结果存在潜在联系。本研究探讨了 NOP2 在肺腺癌 (LUAD) 中的作用，其影响尚不清楚。利用生物信息学，我们评估了来自癌症基因组图谱 (TCGA) 的 513 个 LUAD 和 59 个正常组织样本，以探讨 NOP2 在 LUAD 中的诊断和预后意义。此外，体外实验还比较了 Beas-2b 和 A549 细胞之间的 NOP2 表达。采用先进的数据库和分析工具，包括 LINKEDOMICS、STRING 和 TISIDB，进一步阐明 NOP2 与 LUAD 的关联。我们的研究结果表明，与 Beas-2b 细胞相比，A549 细胞中 NOP2 mRNA 和蛋白的表达显着较高（P  < 0.001）。在 LUAD 中，NOP2 水平升高与总生存期 (OS) 降低和临床分期晚期相关。单变量 Cox 分析显示，NOP2 高表达与 LUAD 中较差的 OS 相关 ( P  < 0.01)，这一发现得到多变量 Cox 分析的独立支持 ( P  < 0.05)。NOP2 表达与 LUAD 风险之间的关系通过列线图呈现。此外，基因集富集分析 (GSEA) 还确定了 7 条 NOP2 相关信号通路。我们研究的一个焦点是 NOP2 与肿瘤免疫相互作用之间的相互作用。值得注意的是，NOP2 表达与 LUAD 中巨噬细胞、中性粒细胞、肥大细胞、自然杀伤 (NK) 细胞和 CD8 + T 细胞的免疫浸润水平呈负相关。此外，NOP2的表达与多种化疗药物的敏感性相关。在体外，我们发现下调NOP2可以减少A549细胞的增殖、迁移和侵袭。此外，NOP2 可以调节 Caspase3 介导的细胞凋亡。总的来说，特别是在预后、免疫浸润和体外实验方面，这些发现表明 NOP2 有可能作为 LUAD 的不良预后生物标志物并加剧肺腺癌细胞的恶性程度。