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Activation-Induced Cytidine Deaminase Promotes Proliferation and Enhances Chemoresistance and Migration in B-cell Lymphoma.
- Source :
-
Anticancer research [Anticancer Res] 2021 Jan; Vol. 41 (1), pp. 237-247. - Publication Year :
- 2021
-
Abstract
- 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.<br />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.<br />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.<br />Conclusion: AID is an important driver of lymphoma, impacting multiple cellular events, and is potentially a strong candidate for targeted therapy in lymphoma.<br /> (Copyright© 2021, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)
- Subjects :
- Animals
Antineoplastic Agents pharmacology
Burkitt Lymphoma drug therapy
Burkitt Lymphoma genetics
Burkitt Lymphoma metabolism
Burkitt Lymphoma pathology
Cell Line, Tumor
Cell Movement genetics
Cell Proliferation
Cytidine Deaminase genetics
DNA Damage
Doxorubicin pharmacology
Ectopic Gene Expression
Enzyme Activation
Gene Expression
Gene Knockdown Techniques
Humans
Lymphoma, B-Cell drug therapy
Lymphoma, B-Cell genetics
Lymphoma, B-Cell pathology
Cytidine Deaminase metabolism
Drug Resistance, Neoplasm
Lymphoma, B-Cell metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1791-7530
- Volume :
- 41
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Anticancer research
- Publication Type :
- Academic Journal
- Accession number :
- 33419818
- Full Text :
- https://doi.org/10.21873/anticanres.14770