Enhanced glycolysis induced by activation of AKT/NF-κB signaling pathway contributes to doxorubicin resistance in DLBCL.

ABSTRACT: Diffuse large B-cell lymphoma (DLBCL), the most prevalent form of lymphoma, is characterized by marked tumor heterogeneity. Treatment failure in DLBCL is often driven by drug resistance, particularly to doxorubicin, and our clinical observations suggest that comorbid type 2 diabetes further increases the incidence of such resistance. However, the intrinsic mechanisms by which altered glucose metabolism modulates doxorubicin resistance in DLBCL cells remain unclear. Here, we demonstrate that aberrant glucose metabolism activates the Protein Kinase B (AKT) signaling pathway, which in turn amplifies Nuclear Factor-kappa B (NF-κB) signaling, thereby promoting doxorubicin resistance. Comparative analyses of sensitive, primary-resistant, and acquired-resistant DLBCL cell lines revealed distinct

SUBMITTER: Wu Y 

PROVIDER: S-EPMC12531284 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature