Zhang Jie, Gao Ting, Chen Shan, Wu Shuang, Mao Yong, Cai Dongyan, Lu Tingxun
Wuxi School of Medicine, Jiangnan University, Wuxi, Jiangsu Province, 214122, China.
Department of Oncology, Affiliated Hospital of Jiangnan University, No.1000, Hefeng Road, Wuxi, Jiangsu Province, 214122, P.R. China.
Ann Hematol. 2025 Apr 5. doi: 10.1007/s00277-025-06321-1.
Diffuse large B-cell lymphoma (DLBCL) is a leading cause of morbidity and mortality among lymphomas in adults, with tumor cells undergoing metabolic reprogramming linked to the immune microenvironment. This study explored the relationship between lactate metabolism-related genes (LMRGs), DLBCL prognosis, and immune microenvironment interactions. Publicly available datasets (GSE10846 and GSE87371) were analyzed, with LMRGs identified using Cox regression and LASSO regression. A risk prognosis model comprising five LMRGs was developed, showing that high-risk patients had worse outcomes due to adverse clinical features, aggressive immune microenvironments, and poor treatment responses. A nomogram combining the model with clinical data predicted 1-, 3-, and 5-year survival. Single-cell RNA sequencing indicated that high LMRG risk scores in B cells may promote immunosuppression via the MIF-CD74/CXCR4 pathway. Functional validation revealed that SDHA knockdown reduced DLBCL cell proliferation in U2932 and KIS-1 cell lines. This LMRG-based model serves as a valuable tool for predicting survival, immune landscape, and clinical risk stratification in DLBCL patients, while also highlighting the crucial role of lactate metabolism in DLBCL pathogenesis. Furthermore, these findings underscore the potential of LMRGs risk scores to guide personalized therapies and improve treatment outcomes.
弥漫性大B细胞淋巴瘤(DLBCL)是成人淋巴瘤发病和死亡的主要原因,其肿瘤细胞经历与免疫微环境相关的代谢重编程。本研究探讨了乳酸代谢相关基因(LMRGs)、DLBCL预后与免疫微环境相互作用之间的关系。分析了公开可用的数据集(GSE10846和GSE87371),使用Cox回归和LASSO回归鉴定LMRGs。开发了一个包含五个LMRGs的风险预后模型,结果显示高危患者由于不良临床特征、侵袭性免疫微环境和较差的治疗反应而预后较差。将该模型与临床数据相结合的列线图可预测1年、3年和5年生存率。单细胞RNA测序表明,B细胞中高LMRG风险评分可能通过MIF-CD74/CXCR4途径促进免疫抑制。功能验证显示,敲低SDHA可降低U2932和KIS-1细胞系中DLBCL细胞的增殖。这种基于LMRG的模型是预测DLBCL患者生存率、免疫格局和临床风险分层的有价值工具,同时也突出了乳酸代谢在DLBCL发病机制中的关键作用。此外,这些发现强调了LMRGs风险评分指导个性化治疗和改善治疗结果的潜力。