Prostate cancer (PCa), characterized by high invasion, metastasis, and recurrence, is the most prevalent malignant tumor in men worldwide. A clear understanding of the underlying molecular mechanisms and their role during PCa tumorigenesis can help develop prognostic and targeted therapies. We analyzed datasets from public databases, including the Cancer Genome Atlas (TCGA) and Oncomine and Gene Expression Profiling Interactive Analysis for differential expression of solute carrier family 16 member 5 (SLC16A5). We further investigated its relationship with clinical stage, pathological grade, and prognosis of PCa. The promoter methylation level of SLC16A5 in PCa was also investigated by UALCAN. We also utilized datasets from UCSC Xena to explore the prognostic role of SLC16A5 methylation levels and CpG site. Correlations between SLC16A5 and immune infiltration were discovered through TIMER. We observed significantly lower levels of SLC16A5 mRNA in PCa relative to normal tissues across six datasets from Oncomine database (p < .001) and 498 cases from TCGA database (p < .0001). SLC16A5 is strongly negatively regulated by its DNA methylation, with a Spearman of −0.81 and Pearson of −0.80 (p < .001). The aberrant SLC16A5 expression resulted in a significant relationship with clinical stage, pathological grade, and lower SLC16A5 mRNA expression, and its hypermethylation was related to a poorer PCa prognosis. SLC16A5 acted as an important factor for PCa diagnosis, with an AUC of 0.9038 (95% CI: 0.8597–0.9479; p < .0001). Besides, the aberrant SLC16A5 expression revealed close correlations with multiple immune cells. Overall, these results indicate that decreased SLC16A5 expression might be a potential biomarker for determining prognosis and immune infiltration in PCa. The positive SLC16A5 modulation might be a promising therapeutic target for PCa.

中文翻译：

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溶质载体家族 16 成员 5 下调及其甲基化可能作为前列腺癌的预后指标

前列腺癌（PCa）以高侵袭、高转移和高复发为特征，是全球男性发病率最高的恶性肿瘤。清楚了解潜在的分子机制及其在 PCa 肿瘤发生过程中的作用有助于开发预后和靶向治疗。我们分析了来自公共数据库的数据集，包括癌症基因组图谱 (TCGA) 和 Oncomine 和基因表达谱交互分析，以了解溶质载体家族 16 成员 5 (SLC16A5) 的差异表达。我们进一步研究了其与PCa临床分期、病理分级和预后的关系。UALCAN 还研究了 PCa 中 SLC16A5 的启动子甲基化水平。我们还利用来自 UCSC Xena 的数据集来探索 SLC16A5 甲基化水平和 CpG 位点的预后作用。通过 TIMER 发现 SLC16A5 与免疫浸润之间的相关性。在 Oncomine 数据库的六个数据集中，我们观察到与正常组织相比，PCa 中 SLC16A5 mRNA 的水平显着降低。p  < .001) 和 TCGA 数据库中的 498 个病例 ( p  < .0001)。SLC16A5 受到其 DNA 甲基化的强烈负调控，Spearman 为 -0.81，Pearson 为 -0.80 (p < .001)。SLC16A5异常表达与临床分期、病理分级和SLC16A5 mRNA表达降低有显着关系，其高甲基化与PCa预后较差有关。SLC16A5 是 PCa 诊断的重要因素，AUC 为 0.9038（95% CI：0.8597–0.9479；p < .0001)。此外，异常的 SLC16A5 表达显示与多种免疫细胞密切相关。总体而言，这些结果表明降低的 SLC16A5 表达可能是确定 PCa 预后和免疫浸润的潜在生物标志物。阳性 SLC16A5 调节可能是 PCa 的一个有希望的治疗靶点。