ArticleiScience2019
MOZ Forms an Autoregulatory Feedback Loop with miR-223 in AML and Monocyte/Macrophage Development.
Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 27 citations in OpenAlex.
- Review
- Macrophage Plasticity: Phenotypic and Functional Profiles Across Pathological Microenvironments.International journal of molecular sciences · 2026Review
- Lysine Acetyltransferase 6A Drives M1 Macrophage Polarization Through Metabolic Reprogramming in Sepsis-Induced Acute Lung Injury.Biomolecules · 2026Article
- Clinical immunology in chromatinopathies: a scoping review.Frontiers in immunology · 2026Article
- Lysine Acetyltransferase 6 in Health and Disease.MedComm · 2025Review
- Immunosuppressive cells in acute myeloid leukemia: mechanisms and therapeutic target.Frontiers in immunology · 2025Review
- Macrophages as Potential Therapeutic Targets in Acute Myeloid Leukemia.Biomedicines · 2024Review
- Immune-dysregulation harnessing in myeloid neoplasms.Cancer medicine · 2024Review
- MiR-223-3p in Cancer Development and Cancer Drug Resistance: Same Coin, Different Faces.International journal of molecular sciences · 2024Review
- Mesenchymal stem cells-macrophages crosstalk and myeloid malignancy.Frontiers in immunology · 2024Review
- Checkpoint Inhibitors in Acute Myeloid Leukemia.Biomedicines · 2023Review
- BRPF1-KAT6A/KAT6B Complex: Molecular Structure, Biological Function and Human Disease.Cancers · 2022Review
- Microenvironmental Features Driving Immune Evasion in Myelodysplastic Syndromes and Acute Myeloid Leukemia.Diseases (Basel, Switzerland) · 2022Review
- Role and Mechanisms of Tumor-Associated Macrophages in Hematological Malignancies.Frontiers in oncology · 2022Review
- MiR-223 as a Regulator and Therapeutic Target in Liver Diseases.Frontiers in immunology · 2022Review
- NanoZnO-modified titanium implants for enhanced anti-bacterial activity, osteogenesis and corrosion resistance.Journal of nanobiotechnology · 2021Review
- Review
- Review
- Macrophages in Acute Myeloid Leukaemia: Significant Players in Therapy Resistance and Patient Outcomes.Frontiers in cell and developmental biology · 2021Review
- The STAT3-miR-223-TGFBR3/HMGCS1 axis modulates the progression of cervical carcinoma.Molecular oncology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Monocytic leukemia zinc-finger protein (MOZ) has been found to form fusion proteins with many regulators in acute myeloid leukemia (AML). However, the molecular functions and underlying mechanism of MOZ in AML is not well understood. Here, clinical MOZ expression analysis combined with data integration from the TCGA and GEO databases indicated that a low level of MOZ was associated with poor prognosis. MOZ knockdown inhibited monocyte differentiation and increased resistance to chemotherapeutic drug-induced apoptosis in THP-1 or U937 cells. In addition, we found that genetic silencing of MOZ suppressed AP-1 and AKT activity in the context of lipopolysaccharide stimulation, resulting in diminished M1 activation of macrophages. We further showed that MOZ was a validated target of miR-223 and functioned as a repressor of miR-223 expression. Our study indicates that a molecular network involving MOZ and miR-223 contributes to the monocyte differentiation and polarization program, which is deregulated in AML.
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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.