简介：目前尚无系统性的泛癌症分析关于PRR7-AS1的作用和调控机制。 方法：本研究采用全面的生物信息学方法挖掘了PRR7-AS1潜在的致癌作用，包括表达状态、预后价值和免疫特征。 结果：我们发现，PRR7-AS1在大多数癌症类型中表达显著上调，并与预后呈负相关。此外，PRR7-AS1表达与大多数肿瘤浸润免疫细胞、免疫得分和泛癌症表达的免疫检查点基因呈反相关。在特定肿瘤中，PRR7-AS1的表达状态与肿瘤突变负荷、微卫星不稳定性和新抗原呈显著相关。与其他公认的生物标志物相比，PRR7-AS1对免疫检查点阻断疗效有最佳预测能力。PRR7-AS1的过表达会影响细胞毒性T细胞介导的抗肿瘤反应。功能富集分析表明，PRR7-AS1可能参与代谢途径。超级增强子活性可能参与了PRR7-AS1表达的调控。我们还构建了PRR7-AS1的竞争性内源性RNA网络。讨论：总体而言，PRR7-AS1具有成为泛癌症诊断、预后和免疫生物标志物的潜力。PRR7-AS1与免疫抑制性微环境相关，并成为免疫治疗的新潜在靶点。表观遗传因素是PRR7-AS1在肿瘤中过表达的驱动力。版权所有 © 2023 Wang，Liu，Li，Liu，Ma，Liu和Li。

Introduction: Systematic pan-cancer analysis of the roles and regulatory mechanisms for PRR7-AS1 is currently not available. Methods: In the present study, a comprehensive bioinformatic approach was used to mine the underlying oncogenic effects of PRR7-AS1, including expression status, prognostic value and immune characteristics. Results: We discovered that PRR7-AS1 expression was remarkably upregulated in most cancer types and exhibited a negative correlation with the prognosis. Furthermore, PRR7-AS1 expression was inversely connected with the majority of tumor-infiltrating immune cells, immune scores and immune checkpoint gene expression in pancancer. There was also a significant correlation between PRR7-AS1 expression status and tumor mutational burden, microsatellite instability, and neoantigens in certain tumors. PRR7-AS1 had the best predictive power for immune checkpoint blockade efficacy compared to other well-recognized biomarkers. PRR7-AS1 overexpression could affect cytotoxic T cells-mediated antitumor responses. Functional enrichment analysis revealed that PRR7-AS1 might be involved in the metabolic pathways. Super enhancer activity might have participated in the regulation of PRR7-AS1 expression. And we constructed the competitive endogenous RNA networks for PRR7-AS1. Discussion: In general, PRR7-AS1 had the potential to be a diagnostic, prognostic and immune biomarker for pan cancer. PRR7-AS1 was correlated with an immunosuppressive microenvironment and was a new potential target for immunotherapy. Epigenetic factors were the driving forces for PRR7-AS1 overexpression in tumors.Copyright © 2023 Wang, Liu, Li, Liu, Ma, Liu and Li.