ArticleLeukemia2014
Silencing AML1-ETO gene expression leads to simultaneous activation of both pro-apoptotic and proliferation signaling.
Article in Leukemia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 75 citations in OpenAlex.
- CXCR4 antagonistic lipid nanoparticles loading siRNA combat refractory AML through AML1-ETO depletion and homoharringtonine sensitization.Materials today. Bio · 2026Article
- Super-Enhancers and Their Parts: From Prediction Efforts to Pathognomonic Status.International journal of molecular sciences · 2024Review
- Cancer fusion transcripts with human non-coding RNAs.Frontiers in oncology · 2024Review
- Article
- Review
- Subtype of Neuroblastoma Cells with High KIT Expression Are Dependent on KIT and Its Knockdown Induces Compensatory Activation of Pro-Survival Signaling.International journal of molecular sciences · 2022Article
- Clinically relevant fusion oncogenes: detection and practical implications.Therapeutic advances in medical oncology · 2022Review
- Mitochondria and Their Relationship with Common Genetic Abnormalities in Hematologic Malignancies.Life (Basel, Switzerland) · 2021Review
- Growth factor signaling predicts therapy resistance mechanisms and defines neuroblastoma subtypes.Oncogene · 2021Article
- Gene Transcription as a Therapeutic Target in Leukemia.International journal of molecular sciences · 2021Review
- Definition of a small core transcriptional circuit regulated by AML1-ETO.Molecular cell · 2021Article
- MicroRNA let-7b downregulates AML1-ETO oncogene expression in t(8;21) AML by targeting its 3'UTR.Experimental hematology & oncology · 2021Article
- RUNX1/RUNX1T1 mediates alternative splicing and reorganises the transcriptional landscape in leukemia.Nature communications · 2021Article
- OGP46 Induces Differentiation of Acute Myeloid Leukemia Cells via Different Optimal Signaling Pathways.Frontiers in cell and developmental biology · 2021Article
- Molecular heterogeneity in breast carcinoma cells with increased invasive capacities.Radiology and oncology · 2020Article
- TAF1 plays a critical role in AML1-ETO driven leukemogenesis.Nature communications · 2019Article
- Elucidation of Novel Therapeutic Targets for Acute Myeloid Leukemias withInternational journal of molecular sciences · 2019Article
- Two Receptors, Two Isoforms, Two Cancers: Comprehensive Analysis of KIT and TrkA Expression in Neuroblastoma and Acute Myeloid Leukemia.Frontiers in oncology · 2019Article
- Article
- Acquired resistance to tyrosine kinase inhibitors may be linked with the decreased sensitivity to X-ray irradiation.Oncotarget · 2018Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The t(8;21)(q22;q22) rearrangement represents the most common chromosomal translocation in acute myeloid leukemia (AML). It results in a transcript encoding for the fusion protein AML1-ETO (AE) with transcription factor activity. AE is considered to be an attractive target for treating t(8;21) leukemia. However, AE expression alone is insufficient to cause transformation, and thus the potential of such therapy remains unclear. Several genes are deregulated in AML cells, including KIT that encodes a tyrosine kinase receptor. Here, we show that AML cells transduced with short hairpin RNA vector targeting AE mRNAs have a dramatic decrease in growth rate that is caused by induction of apoptosis and deregulation of the cell cycle. A reduction in KIT mRNA levels was also observed in AE-silenced cells, but silencing KIT expression reduced cell growth but did not induce apoptosis. Transcription profiling of cells that escape cell death revealed activation of a number of signaling pathways involved in cell survival and proliferation. In particular, we find that the extracellular signal-regulated kinase 2 (ERK2; also known as mitogen-activated protein kinase 1 (MAPK1)) protein could mediate activation of 23 out of 29 (79%) of these upregulated pathways and thus may be regarded as the key player in establishing the t(8;21)-positive leukemic cells resistant to AE suppression.
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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.