ArticleBMC cancer2011
Repression of human activation induced cytidine deaminase by miR-93 and miR-155.
Article in BMC cancer, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 49 citations in OpenAlex.
- A role for host activation-induced cytidine deaminase in innate immune defense against KSHV.PLoS pathogens · 2013Trial
- The power of microRNA regulation-insights into immunity and metabolism.FEBS letters · 2025Review
- SARS-Cov-2 small viral RNA suppresses gene expression via complementary binding to mRNA 3' UTR.microPublication biology · 2024Article
- Article
- 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
- Characterization of a novel sRNA contributing to biofilm formation inmicroPublication biology · 2023Article
- From inflammatory bowel disease to colorectal cancer: what's the role of miRNAs?Cancer cell international · 2022Review
- USP10 regulates B cell response to SARS-CoV-2 or HIV-1 nanoparticle vaccines through deubiquitinating AID.Signal transduction and targeted therapy · 2022Article
- Activation induced cytidine deaminase: An old friend with new faces.Frontiers in immunology · 2022Review
- The Epigenetic Modulation of Cancer and Immune Pathways in Hepatitis B Virus-Associated Hepatocellular Carcinoma: The Influence of HBx and miRNA Dysregulation.Frontiers in immunology · 2021Review
- Activation-induced cytidine deaminase: in sickness and in health.Journal of cancer research and clinical oncology · 2020Review
- Evolutionary effects of the AID/APOBEC family of mutagenic enzymes on human gamma-herpesviruses.Virus evolution · 2019Article
- Epigenetic Priming in Immunodeficiencies.Frontiers in cell and developmental biology · 2019Review
- Epigenomic Modifications Mediating Antibody Maturation.Frontiers in immunology · 2018Review
- Epigenetics of Peripheral B-Cell Differentiation and the Antibody Response.Frontiers in immunology · 2015Review
- The miR-155-PU.1 axis acts on Pax5 to enable efficient terminal B cell differentiation.The Journal of experimental medicine · 2014Article
- miR-93-directed downregulation of DAB2 defines a novel oncogenic pathway in lung cancer.Oncogene · 2014Article
- MicroRNAs in lupus.Autoimmunity · 2014Review
- TGFβR2 is a major target of miR-93 in nasopharyngeal carcinoma aggressiveness.Molecular cancer · 2014Article
- miRNA dysregulation in cancer: towards a mechanistic understanding.Frontiers in genetics · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundActivation Induced cytidine Deaminase (AID) targets the immunoglobulin genes of activated B cells, where it converts cytidine to uracil to induce mutagenesis and recombination. While essential for immunoglobulin gene diversification, AID misregulation can result in genomic instability and oncogenic transformation. This is classically illustrated in Burkitt's lymphoma, which is characterized by AID-induced mutation and reciprocal translocation of the c-MYC oncogene with the IgH loci. Originally thought to be B cell-specific, AID now appears to be misexpressed in several epithelial cancers, raising the specter that AID may also participate in non-B cell carcinogenesis.
methodsThe mutagenic potential of AID argues for the existence of cellular regulators capable of repressing inappropriate AID expression. MicroRNAs (miRs) have this capacity, and we have examined the publically available human AID EST dataset for miR complementarities to the human AID 3'UTR. In this work, we have evaluated the capacity of two candidate miRs to repress human AID expression in MCF-7 breast carcinoma cells.
resultsWe have discovered moderate miR-155 and pronounced miR-93 complementary target sites encoded within the human AID mRNA. Luciferase reporter assays indicate that both miR-93 and miR-155 can interact with the 3'UTR of AID to block expression. In addition, over-expression of either miR in MCF-7 cells reduces endogenous AID protein, but not mRNA, levels. Similarly indicative of AID translational regulation, depletion of either miR in MCF-7 cells increases AID protein levels without concurrent increases in AID mRNA.
conclusionsTogether, our findings demonstrate that miR-93 and miR-155 constitutively suppress AID translation in MCF-7 cells, suggesting widespread roles for these miRs in preventing genome cytidine deaminations, mutagenesis, and oncogenic transformation. In addition, our characterization of an obscured miR-93 target site located within the AID 3'UTR supports the recent suggestion that many miR regulations have been overlooked due to the prevalence of truncated 3'UTR annotations.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.