ArticleOncogene2015
Persistent STAT5 activation in myeloid neoplasms recruits p53 into gene regulation.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
- Dual Functionality of miRNAs During HIV Infection: From Viral Genome Suppression to Immune Response Modulation.Epigenomes · 2026Review
- The E3 ubiquitin ligase Cul5 regulates hematopoietic stem cell function for steady-state hematopoiesis in mice.The Journal of clinical investigation · 2025Article
- Chromothripsis-associated chromosome 21 amplification orchestrates transformation to blast-phase MPN through targetable overexpression of DYRK1A.Nature genetics · 2025Article
- A machine learning-derived immune-related prognostic model identifiesFrontiers in immunology · 2025Article
- TEP RNA: a new frontier for early diagnosis of NSCLC.Journal of cancer research and clinical oncology · 2024Review
- JAK/STAT in leukemia: a clinical update.Molecular cancer · 2024Review
- Genomic and functional impact of Trp53 inactivation in JAK2V617F myeloproliferative neoplasms.Blood cancer journal · 2024Article
- Lifetime Postnatal Exposure to Perfluoroalkyl Substance Mixture and DNA Methylation at Twelve Years of Age.Environmental science & technology letters · 2023Article
- Ancistrocladinium A Induces Apoptosis in Proteasome Inhibitor-Resistant Multiple Myeloma Cells: A Promising Therapeutic Agent Candidate.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Differentiation-related genes in tumor-associated macrophages as potential prognostic biomarkers in non-small cell lung cancer.Frontiers in immunology · 2023Article
- Ectopic JAK-STAT activation enables the transition to a stem-like and multilineage state conferring AR-targeted therapy resistance.Nature cancer · 2022Article
- JAK-STAT core cancer pathway: An integrative cancer interactome analysis.Journal of cellular and molecular medicine · 2022Review
- Enhancement of myogenic differentiation and inhibition of rhabdomyosarcoma progression by miR-28-3p and miR-193a-5p regulated by SNAIL.Molecular therapy. Nucleic acids · 2021Article
- Review
- Janus Kinases in Leukemia.Cancers · 2021Review
- SelectiveToxicology reports · 2021Article
- Analyzing the key gene expression and prognostics values for acute myeloid leukemia.Translational cancer research · 2020Article
- Twins with different personalities: STAT5B-but not STAT5A-has a key role in BCR/ABL-induced leukemia.Leukemia · 2019Article
- Akt and STAT5 mediate naïve human CD4+ T-cell early metabolic response to TCR stimulation.Nature communications · 2019Article
- Combinatorial targeting of XPO1 and FLT3 exerts synergistic anti-leukemia effects through induction of differentiation and apoptosis inHaematologica · 2018Article
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 4 countries.
Funding
Abstract
STAT (Signal Transducer and Activator of Transcription) transcription factors are constitutively activated in most hematopoietic cancers. We previously identified a target gene, LPP/miR-28 (LIM domain containing preferred translocation partner in lipoma), induced by constitutive activation of STAT5, but not by transient cytokine-activated STAT5. miR-28 exerts negative effects on thrombopoietin receptor signaling and platelet formation. Here, we demonstrate that, in transformed hematopoietic cells, STAT5 and p53 must be synergistically bound to chromatin for induction of LPP/miR-28 transcription. Genome-wide association studies show that both STAT5 and p53 are co-localized on the chromatin at 463 genomic positions in proximal promoters. Chromatin binding of p53 is dependent on persistent STAT5 activation at these proximal promoters. The transcriptional activity of selected promoters bound by STAT5 and p53 was significantly changed upon STAT5 or p53 inhibition. Abnormal expression of several STAT5-p53 target genes (LEP, ATP5J, GTF2A2, VEGFC, NPY1R and NPY5R) is frequently detected in platelets of myeloproliferative neoplasm (MPN) patients, but not in platelets from healthy controls. In conclusion, persistently active STAT5 can recruit normal p53, like in the case of MPN cells, but also p53 mutants, such as p53 M133K in human erythroleukemia cells, leading to pathologic gene expression that differs from canonical STAT5 or p53 transcriptional programs.
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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.