ArticleExperimental and therapeutic medicine2025
Excessive activation?induced cytidine deaminase accumulated by proteasome inhibitors rescues abnormal class switch in activated B?cell?like diffuse large B?cell lymphoma.
Article in Experimental and therapeutic medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Investigating the molecular mechanisms of resveratrol in treating diabetic foot ulcers: a comprehensive analysis of network pharmacology and experiment validation.Frontiers in molecular biosciences · 2025Article
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5 authors.
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Abstract
Activation-induced cytidine deaminase (AID) is an enzyme that plays a crucial role in mediating somatic hypermutation and class-switch recombination (CSR). It has been found to be associated with aberrant immunoglobulin CSR in activated B-cell-like diffuse large B-cell lymphoma (ABC-DLBCL). In the present study, MG132, a potent proteasome and calpain inhibitor, induced significant cell death in ABC-DLBCL cells and inhibited the growth of ABC-DLBCL cell xenograft tumors. The results also showed that MG132 induced AID accumulation by impairing proteasome degradation of AID. Excessive endogenous AID accumulation was observed in both AID-deficient and C57/BL6 wild-type mice treated with MG132, and apparent CSR of IgM to IgG1, IgG3 and IgE. Upon stimulation of cytokines such as LPS and/or IL-4, ABC-DLBCL cells also showed a noticeable increase in CSR of IgM to IgG1, IgG3 and IgE with decreased AID protein levels. The present study demonstrates that MG132 can induce AID accumulation, which in turn restores dysfunctional CSR in ABC-DLBCL. Using MG132 as a tool, the present study elucidates the anti-lymphoma effect of proteasome inhibitors on ABC-DLBCL by rescuing the abnormal AID-induced CSR.
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