为探究HMGA2高、低表达对胃癌（gastric cancer, GC）免疫浸润及铁死亡的影响，利用TCGA和GEO数据库中GC转录组数据集，通过TIMER2.0数据库中多种免疫浸润算法开展肿瘤免疫细胞浸润分析，应用DESeq2 R软件包筛选差异表达基因，并基于FerrDb V2数据库分析HMGA2与GC铁死亡的关联。结果表明：HMGA2表达与胃癌中CD8 + T细胞、CD4 + T细胞、B细胞以及Neutrophil细胞浸润相关，HMGA2高表达与低表达的GC之间免疫细胞浸润水平存在显著差异。HMGA2异常表达可能影响GC中钙离子结合、氯离子运输、类固醇激素生物合成和胆固醇代谢等生物学过程。此外，基因TF和SALL4在HMGA2高、低表达组之间的表达显著差异，且与HMGA2表达呈现较强的正相关。Kaplan-Meier生存分析表明，TF和SALL4高表达的GC患者预后较差。同时，研究还发现TF和SALL4的表达与GC免疫及铁死亡显著相关。综上所述，HMGA2高表达和低表达可能对GC免疫和铁死亡产生不同的影响，这有助于深入理解胃癌分子机制，为不同类型GC患者制定更为精准、高效的治疗策略提供指导建议。

To explore the effects of high and low expression of HMGA2 on immune infiltration and ferroptosis in gastric cancer(GC), the transcriptome datasets of GC were download from TCGA and GEO databases. Tumor immune cell infiltration was analyzed using various immune infiltration algorithms in the TIMER2.0 database. Differential expression genes were screened using the DESeq2 R package. The relationship between HMGA2 and GC ferroptosis was analyzed based on the FerrDb V2 database. The expression of HMGA2 is found to be correlated with the infiltration of CD8 + T cells, CD4 + T cells, B cells, and neutrophils in GC. Significant differences in immune cell infiltration levels are observed between GC with high and low HMGA2 expression. Abnormal expression of HMGA2 is suggested to influence cancer-related biological processes and pathways, including calcium ion binding, chloride transport, steroid hormone biosynthesis, and cholesterol metabolism in GC. Additionally, the expression levels of TF and SALL4 are found to differ significantly between the high and low HMGA2 expression groups, and both are strongly positively correlated with HMGA2 expression. Kaplan-Meier survival analysis is performed and reveals that GC patients with high expression of TF or SALL4 are associated with poor prognosis. Furthermore, the expressions of TF and SALL4 are significantly associated with immunity and ferroptosis in GC. In summary, the high and low expression of HMGA2 are considered to exert distinct effects on immunity and ferroptosis in GC, which contributes to a deeper understanding of its molecular mechanisms and provides guidance for the development of more precise and effective therapeutic strategies for different subtypes of GC patients.