ArticleNeoplasia (New York, N.Y.)2020
AID assists DNMT1 to attenuate BCL6 expression through DNA methylation in diffuse large B-cell lymphoma cell lines.
Article in Neoplasia (New York, N.Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Ubiquitin-specific peptidases in lymphoma: a path to novel therapeutics.Frontiers in pharmacology · 2024Pooled it
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- Excessive activation?induced cytidine deaminase accumulated by proteasome inhibitors rescues abnormal class switch in activated B?cell?like diffuse large B?cell lymphoma.Experimental and therapeutic medicine · 2025Article
- Epigenetic Symphony in Diffuse Large B-Cell Lymphoma: Orchestrating the Tumor Microenvironment.Biomedicines · 2025Review
- Activation-induced cytidine deaminase in tertiary lymphoid structures: dual roles and implications in cancer prognosis.Frontiers in oncology · 2025Review
- Epigenetic activation of JAG1 by AID contributes to metastasis of hepatocellular carcinoma.The Journal of biological chemistry · 2025Article
- Advances in epigenetic therapies for B-cell non-hodgkin lymphoma.Annals of hematology · 2024Review
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- Protein phosphatase 2A propels follicular T helper cell development in lupus.Journal of autoimmunity · 2023Article
- Potential Pathogenic Impact of Cow's Milk Consumption and Bovine Milk-Derived Exosomal MicroRNAs in Diffuse Large B-Cell Lymphoma.International journal of molecular sciences · 2023Review
- The off-target effects of AID in carcinogenesis.Frontiers in immunology · 2023Review
- Synthesis and Biological Evaluation of PEGylated MWOMolecules (Basel, Switzerland) · 2022Article
- Transcriptional inhibition of miR-486-3p by BCL6 upregulates Snail and induces epithelial-mesenchymal transition during radiation-induced pulmonary fibrosis.Respiratory research · 2022Article
- Review
- Expression and Clinical Significance of HER2 Gene and DNMT1 in Non-Small-Cell Lung Cancer.Disease markers · 2022Article
- RAG enhances BCR-ABL1-positive leukemic cell growth through its endonuclease activity in vitro and in vivo.Cancer science · 2021Article
- Genetic Polymorphisms in NLRP3 Inflammasome-Associated Genes in Patients with B-Cell Non-Hodgkin's Lymphoma.Journal of inflammation research · 2021Article
- Article
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11 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The BCL6 proto-oncogene encodes a transcriptional repressor, which is required for germinal centers (GCs) formation and lymphomagenesis. Previous studies have been reported that the constitutive expression of BCL6 leads to diffuse large B cell lymphoma (DLBCL) through activation-induced cytidine deaminase (AID) mediated chromosomal translocations and mutations. However, other DLBCLs (45%) without structural variants were characterized by abnormally high level of BCL6 expression through an unknown mechanism. Herein, we report that deficiency in AID or methyltransferase 1 (DNMT1) triggers high level of BCL6 expression. AID-DNMT1 complex binds to -0.4 kb -0 kb region of BCL6 promoter and contributes to generate BCL6 methylation which results in inhibition of BCL6 expression. The proteasome pathway inhibitor MG132 induces accumulation of AID and DNMT1, causes decreased BCL6 expression, and leads to cell apoptosis and tumor growth inhibition in DLBCL cell xenograft mice. These findings propose mechanistic insight into an alternative cofactor role of AID in assisting DNMT1 to maintain BCL6 methylation, thus suppress BCL6 transcription in DLBCL. This novel mechanism will provide a new drug selection in the therapeutic approach to DLBCL in the future.
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