背景：脊髓胶质瘤（SCG）是中枢神经系统（CNS）胶质瘤的一种罕见亚型，代表了神经肿瘤学中的一个复杂挑战。有研究表明，视黄醇脱氢酶10（RDH10）可能是脑胶质瘤的促癌因子，但RDH10在SCG中的生物学作用尚不清楚。方法：我们进行了基因集富集分析（GSEA）和无监督聚类分析，以研究 EMT（上皮间质转化）在胶质瘤中的作用。通过DEG（差异表达基因）筛选和相关性分析，筛选出与SCG EMT过程密切相关的候选基因。通过富集分析和 GSVA（基因集变异分析）研究 RDH10 对 SCG 的潜在机制。通过Trans-well和愈合实验探讨RDH10在SCG侵袭中的作用。采用蛋白质印迹法评估 PI3K-AKT 和 EMT 通路中标志物的水平。进行体内试验验证RDH10在EMT过程中的作用。结果：生物信息分析表明EMT通路与胶质瘤的不良预后相关。进一步分析表明，RDH10与EMT过程的相关性最强。 SCG 组织中视黄醇脱氢酶 10 表达显着增加，与晚期肿瘤分级和不良预后相关。功能分析表明，降低 RDH10 水平会阻碍 SCG 细胞的侵袭和迁移能力，而增加 RDH10 水平则会增强它们。富集分析和蛋白质印迹表明RDH10通过PI3K-AKT途径调节SCG的EMT过程。我们观察到，RDH10 过表达诱导的侵袭能力增强和 EMT 相关蛋白增加可以被 PI3K-AKT 通路抑制剂 (LY294002) 抑制。结论：我们的研究发现RDH10是与SCG的肿瘤分级和预后相关的有效生物标志物。 RDH10可以通过PI3K-AKT途径调节SCG的EMT过程。

Background: Spinal cord glioma (SCG), a rare subset of central nervous system (CNS) glioma, represents a complex challenge in neuro-oncology. There has been research showing that Retinol Dehydrogenase 10 (RDH10) may be a tumor promoting factor in brain glioma, but the biological effects of RDH10 remain undefined in SCG. Methods: We performed gene set enrichment analysis (GSEA) and unsupervised clustering analysis to investigate the roles of EMT (epithelial-mesenchymal transition) in glioma. DEG (differently expressed gene) screening and correlation analysis were conducted to filter the candidate genes which were closely associated with EMT process in SCG. Enrichment analysis and GSVA (Gene Set Variation Analysis) were conducted to investigate the potential mechanism of RDH10 for SCG. Trans-well and healing assay were performed to explore the role of RDH10 in the invasion of SCG. Western blotting was performed to evaluate the levels of markers in PI3K-AKT and EMT pathway. In vivo tests were conducted to verify the role of RDH10 in EMT process. Results: Bioinformatic analysis demonstrated the EMT pathway was associated with dismal prognosis of glioma. Further analysis demonstrated that RDH10 showed the strongest correlation with the EMT process. Retinol Dehydrogenase 10 expression was significantly increased in SCG tissues, correlating with advanced tumor grade and unfavorable prognosis. Functional analysis indicated that decreasing RDH10 levels impeded the invasive and migratory abilities of SCG cells, whereas increasing RDH10 levels augmented them. Enrichment analysis and western blot revealed that RDH10 regulated EMT process of SCG by PI3K-AKT pathway. We observed that the enhanced invasion ability and increased EMT-related protein induced by RDH10 overexpression can be suppressed by PI3K-AKT pathway inhibitor (LY294002). Conclusion: Our research found that RDH10 was an effective biomarker associated with tumor grade and prognosis of SCG. RDH10 could regulate EMT process of SCG through PI3K-AKT pathway.