肾泌尿细胞乳头状癌（KIRP）是一种高度异质性的恶性肿瘤，目前的系统治疗策略难以实现晚期疾病的满意结果。同时，缺乏有效的生物标志物来预测KIRP的预后。使用TCGA、GTEx、UALCAN、TIMER、TIMER 2.0和STRING数据库，我们分析了SNHG6与KIRP亚型、肿瘤浸润免疫细胞和潜在靶向mRNA的关系。基于TCGA数据，进行ROC曲线、Kaplan-Meier生存分析和COX回归分析，评估SNHG6在KIRP中的诊断和预后价值。使用Nomogram预测KIRP患者的3和5年疾病特异性生存率。此外，借助遗传本体论和基因集富集分析，初步探索了SNHG6可能参与的KIRP生物过程和信号通路。在KIRP患者中，SNHG6明显上调，与更侵袭性的亚型（淋巴结受累、病理分期IV、CIMP表型）和糟糕的预后相关。ROC曲线显示良好的诊断效能（AUC值：0.828），Nomogram预测DSS在3年和5年的C指数为0.920（0.898-0.941）。在KIRP的免疫微环境中，SNHG6表达水平与巨噬细胞丰度呈负相关，与癌相关成纤维细胞呈正相关。此外，SNHG6可能通过调节分子的表达，如AURKB、NDC80、UBE2C、NUF2、PTTG1、CENPH、SPC25、CDCA3、CENPM、BIRC5、TROAP、EZH2，促进KIRP的进展。最后，基因集富集分析表明，SNHG6可能参与调节PPAR信号通路和SLIT/ROBO信号通路。我们的分析表明，KIRP中高SNHG6表达状态与患者预后较差有关，并阐明了一些导致这种较差结果的潜在机制。这可能为未来KIRP的治疗和管理提供新的见解。©2023. 作者。

Kidney renal papillary cell carcinoma (KIRP) is a highly heterogeneous malignancy and current systemic therapeutic strategies are difficult to achieve a satisfactory outcome for advanced disease. Meanwhile, there is a lack of effective biomarkers to predict the prognosis of KIRP.Using TCGA, GTEx, UALCAN, TIMER, TIMER 2.0 and STRING databases, we analyzed the relationship of SNHG6 with KIRP subtypes, tumor-infiltrating immune cells and potential target mRNAs. Based on TCGA data, ROC curves, Kaplan-Meier survival analysis and COX regression analysis were performed to evaluate the diagnostic and prognostic value of SNHG6 in KIRP. Nomogram was used to predict 3- and 5-year disease-specific survival in KIRP patients. In addition, with the help of Genetic ontology and Gene set enrichment analysis, the biological processes and signalling pathways that SNHG6 may be involved in KIRP were initially explored.In patients with KIRP, SNHG6 was significantly upregulated and associated with a more aggressive subtype (lymph node involvement, pathological stage IV, CIMP phenotype) and poor prognosis. The ROC curve showed good diagnostic efficacy (AUC value: 0.828) and the C-index of the Nomogram for predicting DSS at 3 and 5 years was 0.920 (0.898-0.941). In the immune microenvironment of KIRP, SNHG6 expression levels were negatively correlated with macrophage abundance and positively correlated with cancer-associated fibroblasts. Furthermore, SNHG6 may promote KIRP progression by regulating the expression of molecules such as AURKB, NDC80, UBE2C, NUF2, PTTG1, CENPH, SPC25, CDCA3, CENPM, BIRC5, TROAP, EZH2. Last, GSEA suggests that SNHG6 may be involved in the regulation of the PPAR signalling pathway and the SLIT/ROBO signalling pathway.Our analysis suggests that a high SNHG6 expression status in KIRP is associated with a poorer prognosis for patients, and also elucidates some potential mechanisms contributing to this poorer outcome. This may provide new insights into the treatment and management of KIRP in the foreseeable future.© 2023. The Author(s).