Activation-Induced Cytidine Deaminase Promotes Proliferation and Enhances Chemoresistance and Migration in B-cell Lymphoma

Background/Aim: Activation-induced cytidine deaminase (AID) is a DNA modifying enzyme which has an essential function in promoting antibody diversification. Its overexpression is strongly associated with B-cell derived malignancies including Burkitt lymphoma, where AID is required for the characteristic c-MYC/IGH translocation. This study aimed at defining AID's oncopathogenic role which is still poorly understood. Materials and Methods: We created over-expressing and knock-down cell culture models of AID, and used cellular assays to provide insight into its contribution to lymphomagenesis. Results: We showed that AID expression is highly specific to, and abundantly expressed in B-cell-derived cancers and that ectopic overexpression of AID leads to rapid cell death. Using a knock-down model, we revealed that AID expression significantly impacts genomic stability, proliferation, migration and drug resistance. Conclusion: AID is an important driver of lymphoma, impacting multiple cellular events, and is potentially a strong candidate for targeted therapy in lymphoma.

Automated summary

The study demonstrated that AID is highly specific to B-cell-derived cancers, with ectopic overexpression leading to rapid cell death, and silencing AID significantly impacting genomic stability, proliferation, migration, and drug resistance. AID is identified as an important driver of lymphoma, affecting multiple cellular events, and potentially a strong candidate for targeted therapy in lymphoma.