ArticleOncotarget2015
Non genomic loss of function of tumor suppressors in CML: BCR-ABL promotes IκBα mediated p53 nuclear exclusion.
Article in Oncotarget, 2015. 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, 20 citations in OpenAlex.
- Human breast milk-derived exosomes attenuate lipopolysaccharide-induced activation in microglia.Journal of neuroinflammation · 2025Article
- HOXA5-Mediated Stabilization of IκBα Inhibits the NF-κB Pathway and Suppresses Malignant Transformation of Breast Epithelial Cells.Cancer research · 2022Article
- Targeting Abnormal Hematopoietic Stem Cells in Chronic Myeloid Leukemia and Philadelphia Chromosome-Negative Classical Myeloproliferative Neoplasms.International journal of molecular sciences · 2021Review
- P53 vs NF-κB: the role of nuclear factor-kappa B in the regulation of p53 activity and vice versa.Cellular and molecular life sciences : CMLS · 2020Review
- Nuclear-cytoplasmic Shuttling in Chronic Myeloid Leukemia: Implications in Leukemia Maintenance and Therapy.Cells · 2019Review
- Overcoming Tyrosine Kinase Inhibitor Resistance in Transformed Cell Harboring SEPT9-ABL1 Chimeric Fusion Protein.Neoplasia (New York, N.Y.) · 2019Article
- Strategies For Targeting Chronic Myeloid Leukaemia Stem Cells.Blood and lymphatic cancer : targets and therapy · 2019Review
- Emerging Non-Canonical Functions and Regulation of p53.International journal of molecular sciences · 2018Article
- Aberrant control of NF-κB in cancer permits transcriptional and phenotypic plasticity, to curtail dependence on host tissue: molecular mode.Cancer biology & medicine · 2017Article
- IκB-α: At the crossroad between oncogenic and tumor-suppressive signals.Oncology letters · 2017Article
- Quantitative Systems Biology to decipher design principles of a dynamic cell cycle network: the "Maximum Allowable mammalian Trade-Off-Weight" (MAmTOW).NPJ systems biology and applications · 2017Review
- Mechanisms of p53 Functional De-Regulation: Role of the IκB-α/p53 Complex.International journal of molecular sciences · 2016Review
- The BCR-ABL/NF-κB signal transduction network: a long lasting relationship in Philadelphia positive Leukemias.Oncotarget · 2016Review
- The non-genomic loss of function of tumor suppressors: an essential role in the pathogenesis of chronic myeloid leukemia chronic phase.BMC cancer · 2016Review
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor suppressor function can be modulated by subtle variation of expression levels, proper cellular compartmentalization and post-translational modifications, such as phosphorylation, acetylation and sumoylation. The non-genomic loss of function of tumor suppressors offers a challenging therapeutic opportunity. The reactivation of a tumor suppressor could indeed promote selective apoptosis of cancer cells without affecting normal cells. The identification of mechanisms that affect tumor suppressor functions is therefore essential. In this work, we show that BCR-ABL promotes the accumulation of the NFKBIA gene product, IκBα, in the cytosol through physical interaction and stabilization of the protein. Furthermore, BCR-ABL/IκBα complex acts as a scaffold protein favoring p53 nuclear exclusion. We therefore identify a novel BCR-ABL/IκBα/p53 network, whereby BCR-ABL functionally inactivates a key tumor suppressor.
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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.