ArticleProceedings of the National Academy of Sciences of the United States of America2010
ATM is down-regulated by N-Myc-regulated microRNA-421.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.
What it found
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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.
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Who cites it
141 citing papers in PubMed, 265 citations in OpenAlex.
- Low expression levels of ATM may substitute for CHEK2 /TP53 mutations predicting resistance towards anthracycline and mitomycin chemotherapy in breast cancer.Breast cancer research : BCR · 2012Trial
- DNA damage response associated miRNA dysregulation in Ataxia-telangiectasia.Molecular biology reports · 2026Article
- Expression of miRNAs Associated With Embryo Development and DNA Damage Response in Porcine Embryos.Molecular reproduction and development · 2025Article
- Review
- Mapping the non-coding RNA landscape in ataxia telangiectasia: a scoping review of ATM dependent miRNA and lncRNA dysregulation.Molecular biology reports · 2025Article
- MicroRNAs: Novel clinical biomarkers for cancer radiotherapy (Review).Molecular medicine reports · 2025Review
- Roots of Progress: Uncovering Cerebellar Ataxias Using iPSC Models.Biomedicines · 2025Review
- The emerging role of miRNAs in biological aging and age-related diseases.Non-coding RNA research · 2025Review
- ATR Inhibition Synergizes With Alkylating PI Polyamide Targeting MYCN by Suppressing DNA Repair in MYCN-Amplified Neuroblastoma.Cancer science · 2025Article
- Adaptive Significance of Non-coding RNAs: Insights from Cancer Biology.Molecular biology and evolution · 2025Review
- A multi-omics approach for biomarker discovery in neuroblastoma: a network-based framework.NPJ systems biology and applications · 2024Article
- Adult Pulmonary Blastoma: A Case Report with Spectrum of Rare Manifestations.Turk patoloji dergisi · 2024Article
- Epigenetic Dysregulation inInternational journal of molecular sciences · 2023Review
- Targeting MALAT1 Augments Sensitivity to PARP Inhibition by Impairing Homologous Recombination in Prostate Cancer.Cancer research communications · 2023Article
- Unraveling Therapeutic Opportunities and the Diagnostic Potential of microRNAs for Human Lung Cancer.Pharmaceutics · 2023Review
- Application of nano-radiosensitizers in combination cancer therapy.Bioengineering & translational medicine · 2023Review
- Accumulation of DNA damage alters microRNA gene transcription in Arabidopsis thaliana.BMC plant biology · 2022Article
- The Dysregulation of MicroRNAs in the Development of Cervical Pre-Cancer-An Update.International journal of molecular sciences · 2022Review
- Article
- Role of MicroRNAs in Neuroendocrine Prostate Cancer.Non-coding RNA · 2022Review
81 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Ataxia-telangiectasia mutated (ATM) is a high molecular weight protein serine/threonine kinase that plays a central role in the maintenance of genomic integrity by activating cell cycle checkpoints and promoting repair of DNA double-strand breaks. Little is known about the regulatory mechanisms for ATM expression itself. MicroRNAs are naturally existing regulators that modulate gene expression in a sequence-specific manner. Here, we show that a human microRNA, miR-421, suppresses ATM expression by targeting the 3'-untranslated region (3'UTR) of ATM transcripts. Ectopic expression of miR-421 resulted in S-phase cell cycle checkpoint changes and an increased sensitivity to ionizing radiation, creating a cellular phenotype similar to that of cells derived from ataxia-telangiectasia (A-T) patients. Blocking the interaction between miR-421 and ATM 3'UTR with an antisense morpholino oligonucleotide rescued the defective phenotype caused by miR-421 overexpression, indicating that ATM mediates the effect of miR-421 on cell cycle checkpoint and radiosensitivity. Overexpression of the N-Myc transcription factor, an oncogene frequently amplified in neuroblastoma, induced miR-421 expression, which, in turn, down-regulated ATM expression, establishing a linear signaling pathway that may contribute to N-Myc-induced tumorigenesis in neuroblastoma. Taken together, our findings implicate a previously undescribed regulatory mechanism for ATM expression and ATM-dependent DNA damage response and provide several potential targets for treating neuroblastoma and perhaps A-T.
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Registered trials
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.