ArticleBlood2020
E2A-PBX1 functions as a coactivator for RUNX1 in acute lymphoblastic leukemia.
Article in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- A Brief Review on the Role of the Transcription Factor PBX1 in Hematologic Malignancies.International journal of molecular sciences · 2025Review
- Biomolecular condensates in immune cell fate.Nature reviews. Immunology · 2025Review
- Long Circulating RNAs Packaged in Extracellular Vesicles: Prospects for Improved Risk Assessment in Childhood B-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2025Article
- Integrated multi-omics analysis of PBX1 in mouse adult neural stem- and progenitor cells identifies a transcriptional module that functionally links PBX1 to TCF3/4.Nucleic acids research · 2024Article
- The advances of E2A-PBX1 fusion in B-cell acute lymphoblastic Leukaemia.Annals of hematology · 2024Review
- Targeting TNF/IL-17/MAPK pathway in hHaematologica · 2024Article
- TAF2, within the TFIID complex, regulates the expression of a subset of protein-coding genes.Cell death discovery · 2024Article
- 1q amplification and PHF19 expressing high-risk cells are associated with relapsed/refractory multiple myeloma.Nature communications · 2024Article
- Comprehensive summary: the role of PBX1 in development and cancers.Frontiers in cell and developmental biology · 2024Review
- PBX1: a TALE of two seasons-key roles during development and in cancer.Frontiers in cell and developmental biology · 2024Review
- Age-related promoter-switch regulates Runx1 expression in adult rat hearts.BMC cardiovascular disorders · 2023Article
- Recent Advances in Transcription Factors Biomarkers and Targeted Therapies Focusing on Epithelial-Mesenchymal Transition.Cancers · 2023Review
- The Role of CREBBP/EP300 and Its Therapeutic Implications in Hematological Malignancies.Cancers · 2023Review
- Spindle function and Wnt pathway inhibition by PBX1 to suppress tumor progression via downregulating DCDC2 in colorectal cancer.Oncogenesis · 2023Article
- Securing access to a comprehensive diagnostic panel for children with suspected acute lymphoblastic leukemia: Results from the Mexico in Alliance with St. Jude "Bridge Project".Frontiers in oncology · 2023Article
- The role of E2A in ATPR-induced cell differentiation and cycle arrest in acute myeloid leukaemia cells.Journal of cellular and molecular medicine · 2022Article
- USP7 facilitates SMAD3 autoregulation to repress cancer progression in p53-deficient lung cancer.Cell death & disease · 2021Article
- Mediator subunit MED1 is required for E2A-PBX1-mediated oncogenic transcription and leukemic cell growth.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- RUNX1 Upregulates CENPE to Promote Leukemic Cell Proliferation.Frontiers in molecular biosciences · 2021Article
- BAHCC1 binds H3K27me3 via a conserved BAH module to mediate gene silencing and oncogenesis.Nature genetics · 2020Article
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Authors and funding
11 authors at 4 institutions in 4 countries.
Funding
Abstract
E2A, a basic helix-loop-helix transcription factor, plays a crucial role in determining tissue-specific cell fate, including differentiation of B-cell lineages. In 5% of childhood acute lymphoblastic leukemia (ALL), the t(1,19) chromosomal translocation specifically targets the E2A gene and produces an oncogenic E2A-PBX1 fusion protein. Although previous studies have shown the oncogenic functions of E2A-PBX1 in cell and animal models, the E2A-PBX1-enforced cistrome, the E2A-PBX1 interactome, and related mechanisms underlying leukemogenesis remain unclear. Here, by unbiased genomic profiling approaches, we identify the direct target sites of E2A-PBX1 in t(1,19)-positive pre-B ALL cells and show that, compared with normal E2A, E2A-PBX1 preferentially binds to a subset of gene loci cobound by RUNX1 and gene-activating machineries (p300, MED1, and H3K27 acetylation). Using biochemical analyses, we further document a direct interaction of E2A-PBX1, through a region spanning the PBX1 homeodomain, with RUNX1. Our results also show that E2A-PBX1 binding to gene enhancers is dependent on the RUNX1 interaction but not the DNA-binding activity harbored within the PBX1 homeodomain of E2A-PBX1. Transcriptome analyses and cell transformation assays further establish a significant RUNX1 requirement for E2A-PBX1-mediated target gene activation and leukemogenesis. Notably, the RUNX1 locus itself is also directly activated by E2A-PBX1, indicating a multilayered interplay between E2A-PBX1 and RUNX1. Collectively, our study provides the first unbiased profiling of the E2A-PBX1 cistrome in pre-B ALL cells and reveals a previously unappreciated pathway in which E2A-PBX1 acts in concert with RUNX1 to enforce transcriptome alterations for the development of pre-B ALL.
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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.