二硫键下垂是一种新的细胞死亡模式，是由于溶质载体家族 7 成员 11 (SLC7A11) 介导的细胞膜胱氨酸转运系统异常而导致的细胞内二硫键积累的程序性模式。大量研究证实了SLC7A11在肿瘤中发挥的突出作用，但SLC7A11作为二硫键死亡的重要介质参与肺腺癌细胞死亡过程仍不清楚。我们获得了4,107个SLC7A11相关基因，并使用总共1,040个样本进行了分析。来自癌症基因组图谱 (TCGA) 队列和 GEO (基因表达综合) 队列的肺腺癌转录组测序数据以及 991 个相关临床数据。首先，我们筛选差异基因并鉴定分子亚型，以评估 SLC7A11 相关基因影响下肺腺癌亚型之间的特征差异。然后，构建风险评分模型来评估肺腺癌患者的预后、免疫浸润、肿瘤微环境和药物治疗效果。最后，我们还使用单细胞数据库分析了肿瘤内细胞类型的分布和特征基因的表达。此外，还预测了相关的药物敏感性。我们筛选了956个具有显着差异的基因，鉴定了2个分子亚型，发现它们的预后存在显着差异，其中B亚型的生存预后明显好于A亚型。此外，我们发现相关通路具有细胞增殖分裂和DNA修复作用的DNA在高风险A型样本中富集。最后，我们构建了一个强大的风险评分系统，我们的风险分析显示高危肺腺癌的免疫微环境中各种免疫细胞成分和肿瘤基质成分普遍减少，并且免疫细胞具有独特的免疫浸润模式，这是我们对SLC7A11相关基因的综合分析表明二硫下垂在肺腺癌的肿瘤微环境、免疫、临床结果和预后方面具有潜在价值。这些发现可能会增加我们对二硫键死亡作为一种新型细胞死亡范例的理解，并为评估肺腺癌的预后和开发新的诊断和治疗策略提供思路。

Disulfidptosis is a novel mode of cell death, a programmed mode of intracellular disulfide accumulation due to solute carrier family 7 member 11 (SLC7A11)-mediated abnormalities in the cell membrane cystine transport system. Numerous studies have confirmed the prominent role played by SLC7A11 in tumors, but the involvement of SLC7A11 as an important mediator of disulfidptosis in the death process of lung adenocarcinoma cells remains unclear.We obtained 4,107 SLC7A11-related genes and analyzed them using a total of 1,040 lung adenocarcinoma transcriptome sequencing data from The Cancer Genome Atlas (TCGA) cohort and GEO (Gene Expression Omnibus) cohort and 991 relevant clinical data. First, we screened for differential genes and identified molecular subtypes for assessing characteristic differences between lung adenocarcinoma subtypes under the influence of SLC7A11-associated genes. Then, risk score models were constructed to assess the prognosis, immune infiltration, tumor microenvironment, and drug treatment effects in lung adenocarcinoma patients. Finally, we also analyzed the distribution of cell types and expression of characteristic genes within the tumor using a single-cell database. In addition, relevant drug sensitivities were predicted.We screened 956 genes with significant differences and identified 2 molecular subtypes and found significant differences in their prognosis and that subtype B had a significantly better survival prognosis than subtype A. In addition, we found that pathways associated with cell proliferation division and DNA repair were enriched in the high-risk type A samples. Finally, we constructed a robust risk-scoring system, and our risk analysis revealed a general reduction of various immune cell components and tumor stromal components in the immune microenvironment of high-risk lung adenocarcinoma and a distinct immune infiltration pattern of immune cells, which was associated with a lower survival rate.Our comprehensive analysis of SLC7A11-related genes suggests that disulfidptosis has a potential value in the tumor microenvironment, immunity, clinical outcome, and prognosis of lung adenocarcinoma. These findings may increase our understanding of disulfidptosis as a novel cell death paradigm and provide ideas for assessing the prognosis of lung adenocarcinoma and developing new diagnostic and therapeutic strategies.