Xu Lili, Wu Jianchun, Tian Jianhui, Zhang Bo, Zhao Yang, Zhao Zhenyu, Luo Yingbin, Li Yan
Clinical Medical Center of Oncology, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Department of Emergency, Shanghai Municipal Hospital of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
J Cell Mol Med. 2025 Apr;29(7):e70435. doi: 10.1111/jcmm.70435.
TME is a core player in the development of a cancerous lesion, the immune evasive potential of the lesion, and its response to therapy. Sphingolipid metabolism, which governs a number of cellular processes, has been recognised as a player involved in the control of immune heterogeneity within the TME. Sphingolipid metabolism-related genes prevalent in the TME of LUAD and LUSC were identified using transcriptomic analysis and clinical samples from the TCGA and GTEx databases. Lasso regression and survival SVM in the Etra Application were employed as machine learning algorithms to determine patient outcomes and to reveal key immune factors associated with gene expression and chemotherapeutic response. Gene expression in lung cancer cells was explored through scRNA-seq data. Thereafter, mediation impact analysis was further performed to explain the defined relation between the immune cell subsets and sphingolipid metabolites and their risk impact on lung cancers. Genes involved in sphingolipid metabolism were dysregulated in lung cancer, correlating with immune cell infiltration and TME remodelling. Lasso regression identified ASAH1 and SMPD1 as strong prognostic markers. scRNA-seq revealed higher gene expression in T cells, macrophages and fibroblasts. Sphingomyelin partially mediated the link between T lymphocyte abundance and lung cancer risk. High-risk phenotypes exhibited enhanced immune evasion via altered regulatory T cell and macrophage polarisation. This research highlights the contribution of sphingolipid metabolism in shaping the TME and its implications for immunotherapy.
肿瘤微环境(TME)在癌性病变的发展、病变的免疫逃逸潜力及其对治疗的反应中起着核心作用。鞘脂代谢控制着许多细胞过程,已被认为是参与控制TME内免疫异质性的一个因素。利用转录组分析以及来自TCGA和GTEx数据库的临床样本,确定了肺腺癌(LUAD)和肺鳞癌(LUSC)的TME中普遍存在的鞘脂代谢相关基因。在Etra应用程序中,套索回归和生存支持向量机被用作机器学习算法,以确定患者的预后,并揭示与基因表达和化疗反应相关的关键免疫因子。通过单细胞RNA测序(scRNA-seq)数据探索肺癌细胞中的基因表达。此后,进一步进行中介影响分析,以解释免疫细胞亚群与鞘脂代谢物之间的既定关系及其对肺癌的风险影响。参与鞘脂代谢的基因在肺癌中表达失调,与免疫细胞浸润和TME重塑相关。套索回归确定ASAH1和SMPD1为强有力的预后标志物。scRNA-seq显示T细胞、巨噬细胞和成纤维细胞中的基因表达较高。鞘磷脂部分介导了T淋巴细胞丰度与肺癌风险之间的联系。高风险表型通过改变调节性T细胞和巨噬细胞极化表现出增强的免疫逃逸。这项研究突出了鞘脂代谢在塑造TME中的作用及其对免疫治疗的意义。