ArticleFrontiers in cell and developmental biology2025
Cholesterol metabolic reprogramming drives the onset of DLBCL and represents a promising therapeutic target.
Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Lipid Metabolism Reprogramming in Diffuse Large B-Cell Lymphoma (DLBCL): Mechanisms and Treatment Strategies.Cancers · 2026Review
- Cholesterol in hematological malignancies: metabolism, mechanisms, and clinical implications.Frontiers in immunology · 2026Review
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Authors and funding
13 authors.
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Abstract
Background: Cholesterol is an essential molecule for tumor cell growth and proliferation, and dysregulated cholesterol metabolism has been widely implicated in cancer pathogenesis. However, the specific role and underlying molecular mechanisms of cholesterol metabolism alterations in diffuse large B-cell lymphoma (DLBCL) remain poorly understood. Methods: We retrospectively analyzed clinical data from 200 DLBCL patients and 185 healthy controls, focusing on lipid and lipoprotein levels, including triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB), and apolipoprotein E (ApoE). Univariate and multivariate Cox proportional hazard models were used to evaluate the prognostic value of these markers, and Kaplan-Meier analysis assessed their associations with overall survival (OS). Bioinformatics analysis predicted associations between lipid markers and cholesterol metabolism. Cellular experiments further investigated the expression of cholesterol metabolism-related proteins and the effect of the cholesterol-depleting agent Methyl-β-cyclodextrin (MβCD) on DLBCL cells. Results: We confirmed significant alterations in metabolic markers (such as TC and ApoA1) between the healthy control group and patients, which were significantly associated with patient prognosis and overall OS. Bioinformatics analysis revealed a strong correlation between these markers and elevated CD36 expression. In addition, DLBCL cells exhibited increased expression of cholesterol uptake and synthesis proteins (CD36, SREBP2, and HMGCR) and decreased expression of efflux proteins (APOA1, NR1H2 and ABCG1), consistent with cholesterol metabolic reprogramming. Treatment with MβCD disrupted CD36 expression and cholesterol metabolism, leading to reduced DLBCL cell survival. Conclusion: These findings underscore the pivotal role of cholesterol metabolic reprogramming in DLBCL progression. CD36 and related metabolic markers represent promising therapeutic targets, opening novel avenues for the treatment of this malignancy.
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