长链非编码RNA（LncRNA）在前列腺癌（PCa）患者中出现紫杉醇耐药（DR）的方式中非常重要。使用来自TCGA和ESTIMATE算法的与PCa相关的表达数据计算了ImmuneScore和StromalScore。通过在ImmuneScore和StromalScore中的DEGs剖析患者的DEGs，我们最终发现了与患者免疫系统和基质相关的DEGs。 CancerSubtypes算法鉴定了与预后相关的PCa亚型，而GSVA评估了它们的通路活性。采用UniCox回归分析来鉴定与预后相关的差异基因集。随后，采用交集分析来确定免疫和预后（IP）相关基因（IPGs）。采用长链非编码RNA（lncRNAs）和IPGs的共表达来确定IP相关lncRNAs（IPLs）。使用SVM-RFE、随机森林和LASSO等三种方法在GEO数据库中寻找重叠的基因。然后建立一个ROC曲线来验证基因标志。使用CIBERSORT技术查看基因标记与免疫细胞之间是否可能存在联系。使用miRDB和TargetScan数据库中的lncRNA-miRNA对和miRNA-mRNA对构建了ERVH48-1-miR-4784-WNT2B ceRNA调控网络。紫杉醇浓度提高了ERVH48-1的表达。ERVH48-1的过表达增加了PCa-DR细胞的增殖、侵袭和迁移，同时抑制了凋亡。ERVH48-1增加了裸鼠中PCa-DR细胞的肿瘤形成性。ERVH48-1作为ceRNA通过靶向miR-4784增加WNT2B的表达。ICG001疗法通过抑制ERVH48-1增加了PCa-DR细胞中Wnt/β-catenin信号通路的活性。最后，ERVH48-1通过miR-4784/Wnt/β-catenin途径以WNT2B依赖的方式增加了紫杉醇耐药性。

Long noncoding RNAs (LncRNAs) are very important in the way that docetaxel resistance (DR) happens in prostate cancer (PCa) patients. ImmuneScore and StromalScore were calculated using PCa-related expression data from TCGA and the ESTIMATE algorithm. We finally found the DEGs that were related to the immune system and the stroma of the patients by making profiles of the DEGs in ImmuneScore and StromalScore. The CancerSubtypes algorithm identified prognosis-related PCa subtypes, and the GSVA assessed their pathway activity. A UniCox regression analysis was used to identify a prognosis-related differential gene set. We then used intersection analysis to identify immunological and prognostic (IP)-related genes (IPGs). The coexpression of long noncoding RNAs (lncRNAs) and IPGs was used to identify IP-related lncRNAs (IPLs). Three methods (SVM-RFE, random forest, and LASSO) were used to find genes that overlap in the GEO database. A gene signature was then validated by building an ROC curve. CIBERSORT technology was used to look at the possibility of a link between the gene signature and immune cells. LncRNA-miRNA pairs and miRNA-mRNA pairs from the miRDB and TargetScan databases were used to construct the ERVH48-1-miR-4784-WNT2B ceRNA regulation network. The concentration of docetaxel elevated the expression of ERVH48-1. Overexpression of ERVH48-1 increased PCa-DR cell proliferation, invasion, and migration while inhibiting apoptosis. ERVH48-1 increased the tumorigenicity of PCa-DR cells in nude mice. ERVH48-1, acting as a ceRNA, targeted miR-4784 to increase WNT2B expression. ICG001 therapy increased Wnt/-catenin signaling activity in PCa-DR cells by inhibiting ERVH48-1. Finally, ERVH48-1 increased docetaxel resistance in a WNT2B-dependent manner via the miR-4784/Wnt/-catenin pathway.