本研究旨在基于患者数据集和全癌分析研究CXCL基因在透明细胞肾细胞癌(ccRCC)中的临床意义、生物功能和潜在机制。还评估了CXCL基因在ccRCC中与免疫成分的相互作用，特别是与中性粒细胞招募和极化机制的关系。此外，利用中性粒细胞极化的签名开发了一个风险评分。通过体外实验评估了CXCL2的作用。结果显示，五个CXCL基因(CXCL 2、5、9、10和11)在肾癌组织中上调，而七个基因(CXCL 1、2、3、5、8、13和14)对患者的生存状况有显著影响。此外，CXCL 1、5和13对无进展生存期有影响。此外，mRNA表达和免疫成分的差异影响了肾癌的结果。此外，通过单细胞和全癌分析，确定了三对CXCL基因-免疫细胞相互作用(CXCL13-CD8+ T细胞，CXCL9/10-M1细胞，CXCL1/2/3/8-中性粒细胞)。使用11个基因和一个TAN签名构建了对KIRC患者具有预后价值的TAN风险评分。中性粒细胞极化显著影响生存率。值得注意的是，CXCL2参与了中性粒细胞的招募和极化，从而促进了ccRCC的进展。总之，鉴定了七个ccRCC患者的预后CXCL基因(CXCL 1/2/3/5/8/13/14)和三对CXCL基因-免疫细胞相互作用。此外，结果表明CXCL 2通过中性粒细胞的招募和极化促进了ccRCC的进展。

This study aimed to investigate the clinical significance, biological functions, and underlying mechanisms of CXCL genes in clear cell renal cell carcinoma (ccRcc) based on patient datasets and pan-cancer analysis. The interaction between CXCL genes in ccRcc and immune components, particularly in relation to neutrophil recruitment and polarization mechanisms, was also evaluated. Furthermore, a risk score was developed using a signature for neutrophil polarization. The role of CXCL2 was assessed through in vitro experiments. Results showed that five CXCL genes (CXCL 2, 5, 9, 10, and 11) were upregulated in renal cancer tissue, while seven genes (CXCL 1, 2, 3, 5, 8, 13, and 14) significantly impacted patient survival. Moreover, CXCL 1, 5, and 13 affected progression-free survival. Besides, differences in mRNA expression and immune components affected renal cancer outcomes. Furthermore, three pairs of CXCL gene-immune cell interactions (CXCL13-CD8+ T cells, CXCL9/10-M1 cells, CXCL1/2/3/8-neutrophils) were identified through single-cell and pan-cancer analysis. A TAN risk score with prognostic value for KIRC patients was constructed using 11 genes and a TAN signature. Neutrophil polarization significantly impacted survival. Notably, CXCL2 was involved in neutrophil recruitment and polarization, thus promoting ccRcc progression. In conclusion, seven prognostic CXCL genes (CXCL 1/2/3/5/8/13/14) for ccRcc patients and three pairs of CXCL gene-immune cell interactions were identified. Furthermore, results showed that CXCL 2 promotes ccRcc progression through neutrophil recruitment and polarization.