ArticleEMBO reports2018
Che-1 is targeted by c-Myc to sustain proliferation in pre-B-cell acute lymphoblastic leukemia.
Article in EMBO reports, 2018. 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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The trial behind it
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Targeting AATF reprograms the tumor microenvironment and suppresses hepatocellular carcinoma via MIR100HG-TGF-β signaling.Molecular therapy. Oncology · 2026Article
- AATF supports proliferation of glioblastoma cells by sustaining mitochondrial respiration through an NRF-1-dependent mechanism.Cell death & disease · 2026Article
- Enhancer engagement sustains oncogenic transformation and progression of B-cell precursor acute lymphoblastic leukemia.Journal of experimental & clinical cancer research : CR · 2024Article
- Profiling the activity of the para-caspase MALT1 in B-cell acute lymphoblastic leukemia for potential targeted therapeutic application.Haematologica · 2024Article
- AATF/Che-1 RNA polymerase II binding protein overexpression reduces the anti-tumor NK-cell cytotoxicity through activating receptors modulation.Frontiers in immunology · 2023Article
- AATF/Che-1 localizes to paraspeckles and suppresses R-loops accumulation and interferon activation in Multiple Myeloma.The EMBO journal · 2022Article
- CK2-mediated phosphorylation of Che-1/AATF is required for its pro-proliferative activity.Journal of experimental & clinical cancer research : CR · 2021Article
- GD2 redirected CAR T and activated NK-cell-mediated secretion of IFNγ overcomes MYCN-dependent IDO1 inhibition, contributing to neuroblastoma cell immune escape.Journal for immunotherapy of cancer · 2021Article
- AATF is Overexpressed in Human Head and Neck Squamous Cell Carcinoma and Regulates STAT3/Survivin Signaling.OncoTargets and therapy · 2021Article
- Che-1/AATF-induced transcriptionally active chromatin promotes cell proliferation in multiple myeloma.Blood advances · 2020Article
- Che-1/AATF binds to RNA polymerase I machinery and sustains ribosomal RNA gene transcription.Nucleic acids research · 2020Article
- Review
- Article
- AATF/Che-1-An RNA Binding Protein at the Nexus of DNA Damage Response and Ribosome Biogenesis.Frontiers in oncology · 2020Review
- B4GALT1 Is a New Candidate to Maintain the Stemness of Lung Cancer Stem Cells.Journal of clinical medicine · 2019Article
- A protein-RNA interaction atlas of the ribosome biogenesis factor AATF.Scientific reports · 2019Article
- Poly-specific neoantigen-targeted cancer vaccines delay patient derived tumor growth.Journal of experimental & clinical cancer research : CR · 2019Article
- MicroRNA-663 antagonizes apoptosis antagonizing transcription factor to induce apoptosis in epithelial cells.Apoptosis : an international journal on programmed cell death · 2019Article
- Recent advances in searching c-Myc transcriptional cofactors during tumorigenesis.Journal of experimental & clinical cancer research : CR · 2018Review
- A new baby in the c-Myc-directed transcriptional machinery: Che-1/AATF.Cell cycle (Georgetown, Tex.) · 2018Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite progress in treating B-cell precursor acute lymphoblastic leukemia (BCP-ALL), disease recurrence remains the main cause of treatment failure. New strategies to improve therapeutic outcomes are needed, particularly in high-risk relapsed patients. Che-1/AATF (Che-1) is an RNA polymerase II-binding protein involved in proliferation and tumor survival, but its role in hematological malignancies has not been clarified. Here, we show that Che-1 is overexpressed in pediatric BCP-ALL during disease onset and at relapse, and that its depletion inhibits the proliferation of BCP-ALL cells. Furthermore, we report that c-Myc regulates Che-1 expression by direct binding to its promoter and describe a strict correlation between Che-1 expression and c-Myc expression. RNA-seq analyses upon Che-1 or c-Myc depletion reveal a strong overlap of the respective controlled pathways. Genomewide ChIP-seq experiments suggest that Che-1 acts as a downstream effector of c-Myc. These results identify the pivotal role of Che-1 in the control of BCP-ALL proliferation and present the protein as a possible therapeutic target in children with relapsed BCP-ALL.
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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.