ArticleNature communications2016
miR-22 has a potent anti-tumour role with therapeutic potential in acute myeloid leukaemia.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
96 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.
- Meta-analysis of the Prognostic Value of microRNA-22 in Leukemia Patients.Technology in cancer research & treatmentPooled it
- CREB1 and GSK3 Isoforms as Potential Adaptive Signaling Nodes in PI3K/Akt/mTOR Inhibitor Treated Philadelphia Chromosome-Positive B-ALL.International journal of molecular sciences · 2026Article
- Downregulation of circulating miR-22 and elevation of serum ATP-citrate lyase in colorectal cancer: a proof-of-concept study.Molecular biology reports · 2026Article
- The Epigenetic Angle in the Precision Medicine Era for Blood Disorder Advancements.Sub-cellular biochemistry · 2026Review
- Extruded nanovesicles derived from umbilical cord mesenchymal stem cells exhibit No tumorigenic potential.Bioactive materials · 2025Article
- TET1: The epigenetic architect of clinical disease progression.Genes & diseases · 2025Review
- Whole-miRNome sequencing: a panel for the targeted sequencing of all human miRNA genes.Nucleic acids research · 2025Article
- Functions, mechanisms, and therapeutic implications of noncoding RNA in acute myeloid leukemia.Fundamental research · 2025Review
- Role of MicroRNAs in Acute Myeloid Leukemia.Genes · 2025Review
- Overexpression of miR-328-3p Inhibits Epithelial-Mesenchymal Transition in Prostate Cancer by Downregulating PFN1.Applied biochemistry and biotechnology · 2025Article
- Deletion of 17p in cancers: Guilt by (p53) association.Oncogene · 2025Review
- Investigating the Impact of LNA-anti-miR-92b, miR-181b, TNF-α, and Piperine on Gene Expression and Cell Viability in Jurkat Cells: Implications for Acute Lymphoblastic Leukemia : LNA-anti- MicroRNAs and Jurkat Cells.Galen medical journal · 2025Article
- Article
- A novel therapeutic strategy: the significance of exosomal miRNAs in acute myeloid leukemia.Medical oncology (Northwood, London, England) · 2024Review
- RNA mGenes & diseases · 2024Article
- The emerging role of microRNA-22 in the Leukemia: experimental and clinical implications.Molecular biology reports · 2023Review
- TET (Ten-eleven translocation) family proteins: structure, biological functions and applications.Signal transduction and targeted therapy · 2023Review
- miR-22-enriched breast cancer cells display repressed glycolytic metabolism, increased glycogen synthesis, and reduced survival in low glucose conditions.Molecular biology reports · 2023Article
- Epigenetic regulation in hematopoiesis and its implications in the targeted therapy of hematologic malignancies.Signal transduction and targeted therapy · 2023Review
- Article
36 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
30 authors at 11 institutions in 4 countries.
Funding
Abstract
MicroRNAs are subject to precise regulation and have key roles in tumorigenesis. In contrast to the oncogenic role of miR-22 reported in myelodysplastic syndrome (MDS) and breast cancer, here we show that miR-22 is an essential anti-tumour gatekeeper in de novo acute myeloid leukaemia (AML) where it is significantly downregulated. Forced expression of miR-22 significantly suppresses leukaemic cell viability and growth in vitro, and substantially inhibits leukaemia development and maintenance in vivo. Mechanistically, miR-22 targets multiple oncogenes, including CRTC1, FLT3 and MYCBP, and thus represses the CREB and MYC pathways. The downregulation of miR-22 in AML is caused by TET1/GFI1/EZH2/SIN3A-mediated epigenetic repression and/or DNA copy-number loss. Furthermore, nanoparticles carrying miR-22 oligos significantly inhibit leukaemia progression in vivo. Together, our study uncovers a TET1/GFI1/EZH2/SIN3A/miR-22/CREB-MYC signalling circuit and thereby provides insights into epigenetic/genetic mechanisms underlying the pathogenesis of AML, and also highlights the clinical potential of miR-22-based AML therapy.
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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.