Cancer cell metabolism including aerobic glycolysis, amino acid and fatty acid metabolism, has been extensively studied. Metabolic reprogramming is a major hallmark of cancer, which promotes cancer cell proliferation, progression and metastasis, as well as provokes resistance to chemotherapeutic drugs. Several signal transduction pathways, such as BCR, MEK/ERK, Notch, NF-κB and PI3K/AKT/mTOR, regulate tumor metabolism, hence promoting tumor cell growth, proliferation and progression. Therefore, targeting metabolic enzymes, metabolites or their signal transduction pathways may constitute a promising therapeutic strategy to enhance cancer treatment efficacy. Diffuse large B-cell lymphoma (DLBCL) is the most aggressive form of non-Hodgkin lymphoma (NHL), and one-third of DLBCL patients suffer from relapsed/refractory disease after chemotherapy. The mechanisms underlying drug resistance are complex, including target gene mutations, metabolic reprogramming, aberrant signal transduction pathways, enhanced drug efflux via overexpression of multidrug efflux transporters like P-glycoprotein, upregulation of anti-apoptotic proteins, drug sequestration and enhanced DND repair. This review delineates the distinct metabolic reprogramming patterns and the association between metabolism and anticancer drug resistance in DLBCL as well as the emerging strategies to surmount chemoresistance in DLBCL.

癌细胞代谢包括有氧糖酵解、氨基酸和脂肪酸代谢，已被广泛研究。代谢重编程是癌症的主要标志，它促进癌细胞增殖、进展和转移，并引起对化疗药物的耐药性。BCR、MEK/ERK、Notch、NF-κB和PI3K/AKT/mTOR等多种信号转导通路调节肿瘤代谢，从而促进肿瘤细胞生长、增殖和进展。因此，靶向代谢酶、代谢物或其信号转导途径可能构成一种有希望的治疗策略，以提高癌症治疗效果。弥漫性大 B 细胞淋巴瘤 (DLBCL) 是最具侵袭性的非霍奇金淋巴瘤 (NHL)，三分之一的 DLBCL 患者在化疗后出现复发/难治性疾病。耐药机制复杂，包括靶基因突变、代谢重编程、异常信号转导通路、通过多药外排转运蛋白（如 P-糖蛋白）过表达增强药物外排、抗凋亡蛋白上调、药物隔离和增强的 DND 修复。本综述描述了 DLBCL 中不同的代谢重编程模式和代谢与抗癌药物耐药性之间的关联，以及克服 DLBCL 中化学耐药性的新兴策略。药物隔离和增强的DND修复。本综述描述了 DLBCL 中不同的代谢重编程模式和代谢与抗癌药物耐药性之间的关联，以及克服 DLBCL 中化学耐药性的新兴策略。药物隔离和增强的DND修复。本综述描述了 DLBCL 中不同的代谢重编程模式和代谢与抗癌药物耐药性之间的关联，以及克服 DLBCL 中化学耐药性的新兴策略。