ArticlePLoS genetics2016
The PU.1-Modulated MicroRNA-22 Is a Regulator of Monocyte/Macrophage Differentiation and Acute Myeloid Leukemia.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 44 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.
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
44 citing papers in PubMed, 60 citations in OpenAlex.
- Correction: The Janus-faced Nature of miR-22 in Hematopoiesis: Is It an Oncogenic Tumor Suppressor or Rather a Tumor-Suppressive Oncogene?PLoS genetics · 2026Article
- Retraction: The PU.1-Modulated MicroRNA-22 Is a Regulator of Monocyte/Macrophage Differentiation and Acute Myeloid Leukemia.PLoS genetics · 2026Article
- Profile of tRNA-derived short non-coding RNAs during monocyte differentiation and their role in macrophage survival.RNA biology · 2025Article
- microRNA-22 Inhibition Stimulates Mitochondrial Homeostasis and Intracellular Degradation Pathways to Prevent Muscle Wasting.International journal of molecular sciences · 2025Article
- Functions, mechanisms, and therapeutic implications of noncoding RNA in acute myeloid leukemia.Fundamental research · 2025Review
- Unveiling the Role of Histone Methyltransferases in Psoriasis Pathogenesis: Insights from Transcriptomic Analysis.International journal of molecular sciences · 2025Article
- Role of MicroRNAs in Acute Myeloid Leukemia.Genes · 2025Review
- FunCoup 6: advancing functional association networks across species with directed links and improved user experience.Nucleic acids research · 2025Article
- SPI1Journal for immunotherapy of cancer · 2024Article
- A novel therapeutic strategy: the significance of exosomal miRNAs in acute myeloid leukemia.Medical oncology (Northwood, London, England) · 2024Review
- PU.1 induces tumor-associated macrophages promoting glioma progression through BTK-mediated Akt/mTOR pathway activation.American journal of cancer research · 2024Article
- The emerging role of microRNA-22 in the Leukemia: experimental and clinical implications.Molecular biology reports · 2023Review
- Insight into microRNAs' involvement in hematopoiesis: current standing point of findings.Stem cell research & therapy · 2023Review
- Clinical Significance of microRNAs in Hematologic Malignancies and Hematopoietic Stem Cell Transplantation.Cancers · 2023Review
- Epigenetic regulation in hematopoiesis and its implications in the targeted therapy of hematologic malignancies.Signal transduction and targeted therapy · 2023Review
- Review
- Review
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- Dicer deficiency impairs proliferation but potentiates anti-tumoral effect of macrophages in glioblastoma.Oncogene · 2022Article
- MicroRNAs as Regulators of Phagocytosis.Cells · 2022Review
Corrections and comments
- Commented on by
- Retracted
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA-22 (miR-22) is emerging as a critical regulator in organ development and various cancers. However, its role in normal hematopoiesis and leukaemogenesis remains unclear. Here, we detected its increased expression during monocyte/macrophage differentiation of HL-60, THP1 cells and CD34+ hematopoietic stem/progenitor cells, and confirmed that PU.1, a key transcriptional factor for monocyte/macrophage differentiation, is responsible for transcriptional activation of miR-22 during the differentiation. By gain- and loss-of-function experiments, we demonstrated that miR-22 promoted monocyte/macrophage differentiation, and MECOM (EVI1) mRNA is a direct target of miR-22 and MECOM (EVI1) functions as a negative regulator in the differentiation. The miR-22-mediated MECOM degradation increased c-Jun but decreased GATA2 expression, which results in increased interaction between c-Jun and PU.1 via increasing c-Jun levels and relief of MECOM- and GATA2-mediated interference in the interaction, and thus promoting monocyte/macrophage differentiation. We also observed significantly down-regulation of PU.1 and miR-22 as well as significantly up-regulation of MECOM in acute myeloid leukemia (AML) patients. Reintroduction of miR-22 relieved the differentiation blockage and inhibited the growth of bone marrow blasts of AML patients. Our results revealed new function and mechanism of miR-22 in normal hematopoiesis and AML development and demonstrated its potential value in AML diagnosis and 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.