ArticleEMBO reports2005
Bcr-Abl activates the AKT/Fox O3 signalling pathway to restrict transforming growth factor-beta-mediated cytostatic signals.
Article in EMBO reports, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Molecular Mechanisms in Genetic Aortopathy-Signaling Pathways and Potential Interventions.International journal of molecular sciences · 2023Review
- BRD9 inhibition promotes PUMA-dependent apoptosis and augments the effect of imatinib in gastrointestinal stromal tumors.Cell death & disease · 2021Article
- The vascular bone marrow niche influences outcome in chronic myeloid leukemiaHaematologica · 2020Article
- Article
- The role of TGFβ in hematopoiesis and myeloid disorders.Leukemia · 2019Review
- The role of TGF-β/SMAD4 signaling in cancer.International journal of biological sciences · 2018Review
- Regulation of Bim in Health and Disease.Oncotarget · 2015Review
- c-Abl-dependent molecular circuitry involving Smad5 and phosphatidylinositol 3-kinase regulates bone morphogenetic protein-2-induced osteogenesis.The Journal of biological chemistry · 2013Article
- TGF-β - an excellent servant but a bad master.Journal of translational medicine · 2012Review
- Transforming growth factor-β and the hallmarks of cancer.Cellular signalling · 2011Review
- The research on the immuno-modulatory defect of mesenchymal stem cell from Chronic Myeloid Leukemia patients.Journal of experimental & clinical cancer research : CR · 2011Article
- VE-cadherin Regulates Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia Sensitivity to Apoptosis.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2010Article
- Gene expression signatures in polyarticular juvenile idiopathic arthritis demonstrate disease heterogeneity and offer a molecular classification of disease subsets.Arthritis and rheumatism · 2009Article
- Signaling cross-talk between TGF-beta/BMP and other pathways.Cell research · 2009Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fusion of Abl with either Bcr or Tel in human leukaemia leads to the constitutive activation of Abl tyrosine kinase, which in turn induces growth-factor-independent proliferation and cell survival. However, the mechanism by which Bcr-Abl induces cellular transformation has not yet been well characterized. Here, we show that Bcr-Abl-expressing cells are resistant to growth inhibition and apoptosis mediated by transforming growth factor-beta (TGF-beta). Interestingly, we observed that the suppressive effects of Bcr-Abl on TGF-beta responses were not mediated by an impairment of Smad signalling, which is believed to act as the principal mediator of TGF-beta responses. In contrast, we found that Bcr-Abl can target the protein kinase AKT and the transcription factor Fox O3 to interfere with growth inhibition and apoptosis in response to TGF-beta. Our results show a novel mechanism of cellular transformation by the oncogenic fusion protein Bcr-Abl through suppression of the cytostatic actions of TGF-beta.
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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.