ArticleProceedings of the National Academy of Sciences of the United States of America2013
Activation-induced cytidine deaminase (AID) is necessary for the epithelial-mesenchymal transition in mammary epithelial cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- Evolutionary Comparative Analyses of DNA-Editing Enzymes of the Immune System: From 5-Dimensional Description of Protein Structures to Immunological Insights and Applications to Protein Engineering.Frontiers in immunology · 2021Pooled it
- Super-enhancer profiling reveals ThPOK/ZBTB7B, a CD4Cellular and molecular life sciences : CMLS · 2025Article
- Plumbagin targets the GLUT1/MMP-2 axis to inhibit oral squamous cell carcinoma progression.Cancer cell international · 2025Article
- Molecular Insights into Phytochemicals Mediated Epigenetic Regulation in Preclinical Models of Breast Cancer.Drug design, development and therapy · 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
- B-1 derived anti-Thy-1 B cells in old aged mice develop lymphoma/leukemia with high expression of CD11b and Hamp2 that different from TCL1 transgenic mice.Immunity & ageing : I & A · 2024Article
- Genomic and microenvironmental heterogeneity shaping epithelial-to-mesenchymal trajectories in cancer.Nature communications · 2023Article
- The off-target effects of AID in carcinogenesis.Frontiers in immunology · 2023Review
- From inflammatory bowel disease to colorectal cancer: what's the role of miRNAs?Cancer cell international · 2022Review
- Epigenetics and environment in breast cancer: New paradigms for anti-cancer therapies.Frontiers in oncology · 2022Review
- Structure-Based Design of First-Generation Small Molecule Inhibitors Targeting the Catalytic Pockets of AID, APOBEC3A, and APOBEC3B.ACS pharmacology & translational science · 2021Article
- AID Contributes to Accelerated Disease Progression in the TCL1 Mouse Transplant Model for CLL.Cancers · 2021Article
- CancerFrontiers in immunology · 2021Article
- Activation-induced cytidine deaminase: in sickness and in health.Journal of cancer research and clinical oncology · 2020Review
- Understanding seasonal weight loss tolerance in dairy goats: a transcriptomics approach.BMC genomics · 2020Article
- Lineage plasticity in cancer: a shared pathway of therapeutic resistance.Nature reviews. Clinical oncology · 2020Review
- Identification of Novel MeCP2 Cancer-Associated Target Genes and Post-Translational Modifications.Frontiers in oncology · 2020Article
- AID modulates carcinogenesis network via DNA demethylation in bladder urothelial cell carcinoma.Cell death & disease · 2019Article
- Activation-induced deaminase (AID) localizes to the nucleus in brief pulses.PLoS genetics · 2019Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Activation-induced cytidine deaminase (AID), which functions in antibody diversification, is also expressed in a variety of germ and somatic cells. Evidence that AID promotes DNA demethylation in epigenetic reprogramming phenomena, and that it is induced by inflammatory signals, led us to investigate its role in the epithelial-mesenchymal transition (EMT), a critical process in normal morphogenesis and tumor metastasis. We find that expression of AID is induced by inflammatory signals that induce the EMT in nontransformed mammary epithelial cells and in ZR75.1 breast cancer cells. shRNA-mediated knockdown of AID blocks induction of the EMT and prevents cells from acquiring invasive properties. Knockdown of AID suppresses expression of several key EMT transcriptional regulators and is associated with increased methylation of CpG islands proximal to the promoters of these genes; furthermore, the DNA demethylating agent 5 aza-2'deoxycytidine (5-Aza-dC) antagonizes the effects of AID knockdown on the expression of EMT factors. We conclude that AID is necessary for the EMT in this breast cancer cell model and in nontransformed mammary epithelial cells. Our results suggest that AID may act near the apex of a hierarchy of regulatory steps that drive the EMT, and are consistent with this effect being mediated by cytosine demethylation. This evidence links our findings to other reports of a role for AID in epigenetic reprogramming and control of gene expression.
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