基于脂肪酸代谢基因的胶质瘤预后模型构建及其免疫微环境与药物敏感性研究

doi:10.3877/cma.j.issn.2095-123X.2026.04.002

中华脑科疾病与康复杂志(电子版) ›› 2026, Vol. 16 ›› Issue (04) : 200 -212. doi: 10.3877/cma.j.issn.2095-123X.2026.04.002

临床研究

基于脂肪酸代谢基因的胶质瘤预后模型构建及其免疫微环境与药物敏感性研究

王洪东¹, 张昀昇², 张瑜廉³, 张黎³, 于炎冰³^,^†(

)

¹100029　北京，北京大学中日友好医学院
²100123　北京，民航总医院神经外科
³100029　北京，中日友好医院神经外科

收稿日期:2025-07-18 出版日期:2026-08-15
通信作者: 于炎冰

Construction of a fatty acid metabolism gene-based prognostic model for glioma and investigation of its immune microenvironment and drug sensitivity

Hongdong Wang¹, Yunsheng Zhang², Yulian Zhang³, Li Zhang³, Yanbing Yu³^,^†()

¹Peking University China-Japan Friendship School of Clinical Medicine, Beijing 100029, China
²Department of Neurosurgery, Civil Aviation General Hospital, Beijing 100123, China
³Department of Neurosurgery, China-Japan Friendship Hospital, Beijing 100029, China

Received:2025-07-18 Published:2026-08-15
Corresponding author: Yanbing Yu
Supported by:
National Natural Science Foundation of China(32300816, 32471035); Beijing Natural Science Foundation(L242112); Elite Medical Talent Project of China-Japan Friendship Hospital(ZRJY2024-QM07)

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引用本文：

王洪东, 张昀昇, 张瑜廉, 张黎, 于炎冰. 基于脂肪酸代谢基因的胶质瘤预后模型构建及其免疫微环境与药物敏感性研究[J/OL]. 中华脑科疾病与康复杂志(电子版), 2026, 16(04): 200-212.

Hongdong Wang, Yunsheng Zhang, Yulian Zhang, Li Zhang, Yanbing Yu. Construction of a fatty acid metabolism gene-based prognostic model for glioma and investigation of its immune microenvironment and drug sensitivity[J/OL]. Chinese Journal of Brain Diseases and Rehabilitation(Electronic Edition), 2026, 16(04): 200-212.

目的

探讨脂肪酸代谢相关基因对胶质瘤预后的价值，基于这些基因构建综合模型，分析其与免疫微环境及药物敏感性的关联。

方法

通过癌症基因组图谱（TCGA）数据库获取胶质瘤患者的转录组及临床数据，筛选获得具有完整临床信息和有效生存数据（生存时间>0 d）的胶质母细胞瘤（GBM）和低级别胶质瘤（LGG）样本，纳入肿瘤组。同时，通过TCGA数据库和基因型-组织表达（GTEx）数据库获取正常人脑组织转录组数据，筛选正常样本，纳入正常样本组。脂肪酸代谢相关基因从京都基因与基因组百科全书（KEGG）数据库中提取。采用差异分析与Cox比例风险模型回归筛选出与预后相关的核心脂肪酸代谢基因。按照7∶3的比例采用随机数字表法将胶质瘤患者分为训练集和验证集。利用随机森林算法构建风险评分模型，通过对年龄、性别、种族进行生存分析，筛选出与生存相关的因素，联合甲基化位点水平构建综合列线图。采用共识聚类法将胶质瘤样本分为2个脂肪酸代谢亚型[亚型1（低代谢组），亚型2（高代谢组）]。进一步采用基于标记基因的细胞类型识别算法和癌症药物敏感性基因组学数据库评估免疫浸润特征及药物敏感性，最后通过实时荧光定量聚合酶链式反应验证核心基因在胶质瘤细胞中的表达水平。

结果

共筛选出4个核心脂肪酸代谢相关基因：ACOT2、ACOT4、ACSL5和ADH6。基于这4个基因构建随机森林风险模型，将胶质瘤患者按7∶3随机划分为训练集（422例）和验证集（182例）。该模型在训练集与验证集中均表现稳健，训练集中预测1、3、5年生存率的曲线下面积（AUC）>0.75，验证集中1、3、5年生存率的AUC>0.6。进一步构建的综合列线图预测精度良好，校准曲线R²=0.92。免疫浸润分析显示，胶质瘤组织中M2型巨噬细胞显著富集。药物敏感性分析发现，亚型2对Fluorouracil等药物更为敏感（半数最大抑制浓度降低30%~50%）。细胞实验证实，上述核心基因在胶质瘤中均呈显著高表达（P<0.001）。

结论

基于脂肪酸代谢相关基因（ACOT2、ACOT4、ACSL5、ADH6）、MGMT基因甲基化水平及患者年龄构建的综合模型，能够有效实现胶质瘤的预后分层，为个体化治疗策略的制定提供新的理论依据。

关键词: 胶质瘤, 脂肪酸代谢, 预后模型, 免疫浸润, 药物敏感性

Objective

To investigate the prognostic value of fatty acid metabolism-related genes in glioma, construct a comprehensive model based on these genes, and analyze its associations with the immune microenvironment and drug sensitivity.

Methods

This study integrated transcriptomic and clinical data from The Cancer Genome Atlas (TCGA) and the Genotype Tissue Expression (GTEx) databases. Differentially expressed genes and Cox proportional hazards model regression were first used to screen for core prognostic fatty acid metabolism-related genes. Glioma patients were then randomly divided into a training set and a validation set at a 7:3 ratio. A risk score model was constructed using the random forest algorithm. Survival analysis was performed on age, gender, and race to identify survival-related factors, which were then combined with methylation site levels to develop a comprehensive nomogram. Consensus clustering was subsequently applied to classify glioma samples into two fatty acid metabolism subtypes (subtype 1/low-metabolism group and subtype 2/high-metabolism group). Immune infiltration characteristics and drug sensitivity were evaluated using the CIBERSORT algorithm and the Genomics of Drug Sensitivity in Cancer database. Finally, expression levels of the core genes were validated in glioma cells by real-time quantitative polymerase chain reaction (RT-qPCR).

Results

Four core fatty acid metabolism-related genes were identified: ACOT2, ACOT4, ACLS5, and ADH6. Based on these four genes, a random-forest risk model was constructed, and glioma patients were randomly split into a training set (422 patients) and a validation set (182 patients) in a 7:3 ratio. The model exhibited robust performance in both datasets, with areas under the curve (AUCs) for predicting 1-, 3-, and 5-year survival all greater than 0.75 in the training set and all greater than 0.6 in the validation set. The combined nomogram also exhibited excellent predictive accuracy (calibration curve R²=0.92). Immune infiltration analysis revealed significant enrichment of M2 macrophages in glioma tissues. Drug sensitivity analysis indicated that subtype 2 (high-metabolism group) was more sensitive to agents such as Fluorouracil (with half-maximal inhibitory concentration reduced by 30%-50%). Cell experiments confirmed that the above core genes were significantly overexpressed in glioma (P<0.001).

Conclusions

The comprehensive model based on fatty acid metabolism-related genes (ACOT2, ACOT4, ACSL5, ADH6), MGMT methylation status, and patient age can effectively stratify the prognosis of glioma, providing a new theoretical basis for individualized treatment strategies.

Key words: Glioma, Fatty acid metabolism, Prognostic model, Immune infiltration, Drug sensitivity

图1 正常样本组和肿瘤组DEGs及其差异表达且与预后相关的脂肪酸代谢相关基因的筛选结果A：火山图示胶质瘤组织与正常脑组织间的DEGs，红色和蓝色分别代表显著上调和下调基因（筛选阈值：|log₂FoldChange|>1，P<0.05）；B：热图示差异基因在胶质瘤组织和正常样本中的表达模式，颜色梯度表示标准化后的表达量（红色：高表达；蓝色：低表达）；C：韦恩图示差异表达基因（1616个）、生存相关基因（1378个）及脂肪酸代谢基因（75个）的交集，最终筛选出4个脂肪酸代谢基因（ACOT2、ACOT4、ACSL5、ADH6）；DEG：差异表达基因；ACOT2：酰基辅酶A硫酯酶2；ACOT4：酰基辅酶A硫代酯酶4；ACSL5：酰基辅酶A合成酶长链家族成员5；ADH6：醇脱氢酶6（V类）

Fig.1 Screening results of DEGs and prognosis-associated fatty acid metabolism-related genes between normal and tumor groups

图2 肿瘤组随机森林风险预后模型的构建及变量重要性分析A：模型稳定性分析，即随机森林模型误差率随决策树数量增加的变化趋势，当ntree=500时，模型误差波动逐步收窄，ntree=600时，误差进入稳定平台期，模型性能趋于平稳；B：采用变量重要性评分评估脂肪酸代谢基因对模型预测精度的贡献，即ACSL5、ACOT2、ADH6、ACOT4对模型的重要性（%IncMSE），其中ADH6的%IncMSE最高；C：训练集中脂肪酸代谢基因重要性排序，即ADH6、ACOT4、ACOT2、ACSL5基因在风险评分中的权重系数，其中ADH6贡献度最高；ACOT2：酰基辅酶A硫酯酶2；ACOT4：酰基辅酶A硫代酯酶4；ACSL5：酰基辅酶A合成酶长链家族成员5；ADH6：醇脱氢酶6（V类）

Fig.2 Construction and variable importance analysis of the Random Forest-based prognostic risk model in the glioma cohort

图3 随机森林构建脂肪酸代谢相关基因风险模型的预测效能评估A：训练集中风险模型预测1、3、5年生存率的ROC曲线；B：验证集中风险模型预测1、3、5年生存率的ROC曲线；C~D：Kaplan-Meier生存曲线比较训练集（C）和验证集（D）中高风险组与低风险组的生存差异（Log-rank P<0.0001）；ROC：受试者工作特征；AUC：曲线下面积

Fig.3 Performance evaluation of the fatty acid metabolism-related gene-based risk model constructed using Random Forest

图4 肿瘤组样本临床指标的生存分析A：按年龄中位数分组的Kaplan-Meier生存曲线显示年轻组（≤43岁）生存率显著高于高龄组（>43岁）（Log-rank P<0.0001）；B~C：不同性别（B）和种族（C）分组的Kaplan-Meier生存曲线显示差异均无统计学意义（P>0.05）

Fig.4 Survival analysis of clinical parameters in the tumor cohort

图5 综合预后列线图的构建与效能评估A：整合年龄、MGMT启动子甲基化水平及4个脂肪酸代谢基因（ACOT2、ACOT4、ACSL5、ADH6）表达水平构建综合预后列线图，量化预测胶质瘤患者的生存概率；B：300 d生存概率校准曲线显示，列线图预测的生存概率与实际观测值高度一致（R²=0.92）；C：通过最大选择秩统计量确定列线图总得分的最佳截断点为228.7；D：采用Kaplan-Meier生存曲线进行生存差异验证，结果显示，由列线图评分划分的高、低风险组间预后差异具有统计学意义（Log-rank P<0.0001）；E：决策曲线分析结果显示，在较宽的阈值概率范围内，综合预后列线图的临床净收益显著高于"全治疗"或"无治疗"方案；；ACOT2：酰基辅酶A硫酯酶2；ACOT4：酰基辅酶A硫代酯酶4；ACSL5：酰基辅酶A合成酶长链家族成员5；ADH6：醇脱氢酶6（V类）

Fig.5 Construction and performance evaluation of the integrated prognostic nomogram

图6 胶质瘤免疫浸润特征及其与脂肪酸代谢基因的相关性分析A：胶质瘤与正常脑组织间22种免疫细胞浸润丰度的差异比较小提琴图结果显示，与正常脑组织相比，胶质瘤组织中M2巨噬细胞、中性粒细胞及浆细胞等免疫细胞的浸润水平显著升高；而CD8⁺T细胞和单核细胞在正常组织中的比例相对较高（Benjamini-Hochberg校正^aP<0.05）；B：4个脂肪酸代谢基因与22种免疫细胞浸润水平的相关性热图显示，关键基因（ACOT2、ACOT4、ACSL5、ADH6）与多种免疫细胞浸润显著相关；ACOT2：酰基辅酶A硫酯酶2；ACOT4：酰基辅酶A硫代酯酶4；ACSL5：酰基辅酶A合成酶长链家族成员5；ADH6：醇脱氢酶6（V类）

Fig.6 Immune infiltration characteristics in glioma and their correlation with key fatty acid metabolism genes

图7 基于脂肪酸代谢亚型的胶质瘤药物敏感性预测与分析A~B：胶质瘤脂肪酸代谢亚型鉴定与验证的一致性矩阵热图（A）与累积分布函数曲线（B）；C：不同代谢亚型对6种代表性药物或联合方案的敏感性比较：高代谢组对Ciclopirox、Fluorouracil等6种代表性药物或联合方案的预测IC₅₀值显著低于低代谢组（P<0.001）；IC₅₀：半数最大抑制浓度

Fig.7 Drug sensitivity prediction and analysis in glioma based on fatty acid metabolism subtypes

图8 4个脂肪酸代谢基因在不同胶质瘤细胞系中表达水平的RT-qPCR检测结果A：ACOT2；B：ACOT4；C：ACSL5；D：ADH6；与HA1800比较，^aP<0.05；U118、T98G、U251、A172为人胶质瘤细胞系；HA1800为人正常星形胶质细胞；ACOT2：酰基辅酶A硫酯酶2；ACOT4：酰基辅酶A硫代酯酶4；ACSL5：酰基辅酶A合成酶长链家族成员5；ADH6：醇脱氢酶6（V类）

Fig.8 RT-qPCR validation of the expression levels of four key fatty acid metabolism-related genes in glioma cell lines

表1 脂肪酸代谢相关基因的引物序列

Tab.1 Primer sequences of fatty acid metabolism-related genes

基因	上游引物(5′-3′)	下游引物(3′-5′)
ACOT2	CATCTCCTGCTGTCCTTCG	ATCTGACCAACCTGCCTCA
ACOT4	ATCTTTGGTATTGGAGGGGGC	GCTAGAGCCAACGTGGCAAA
ACSL5	AAGGCATTGGTGCTGATAGG	TCAGGTCTTCTGGGCTAGGA
ADH6	CCTCCTGCAATGAGAGCTATGG	GGATGTGCTGTCTGCTCTTCCA
GAPDH	AACATCATCCCTGCCTCTACTG	TGCTTCACCACCTTCTTGATGT

表1 脂肪酸代谢相关基因的引物序列

Tab.1 Primer sequences of fatty acid metabolism-related genes

基因	上游引物(5′-3′)	下游引物(3′-5′)
ACOT2	CATCTCCTGCTGTCCTTCG	ATCTGACCAACCTGCCTCA
ACOT4	ATCTTTGGTATTGGAGGGGGC	GCTAGAGCCAACGTGGCAAA
ACSL5	AAGGCATTGGTGCTGATAGG	TCAGGTCTTCTGGGCTAGGA
ADH6	CCTCCTGCAATGAGAGCTATGG	GGATGTGCTGTCTGCTCTTCCA
GAPDH	AACATCATCCCTGCCTCTACTG	TGCTTCACCACCTTCTTGATGT

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Construction of a fatty acid metabolism gene-based prognostic model for glioma and investigation of its immune microenvironment and drug sensitivity

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Construction of a fatty acid metabolism gene-based prognostic model for glioma and investigation of its immune microenvironment and drug sensitivity