ArticleLeukemia2009
BCR-ABL promotes neutrophil differentiation in the chronic phase of chronic myeloid leukemia by downregulating c-Jun expression.
Article in Leukemia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- The protein tyrosine phosphatase CD45 promotes PMN transepithelial migration, antimicrobial function, and colonic mucosal repair.JCI insight · 2026Article
- Cancer non-stem cells as a potent regulator of tumor microenvironment: a lesson from chronic myeloid leukemia.Molecular biomedicine · 2021Review
- Kindlin-3 loss curbs chronic myeloid leukemia in mice by mobilizing leukemic stem cells from protective bone marrow niches.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Paradoxical counteraction by imatinib against cell death in myeloid progenitor 32D cells expressing p210BCR-ABL.Oncotarget · 2018Article
- Increased peroxisome proliferator-activated receptor γ activity reduces imatinib uptake and efficacy in chronic myeloid leukemia mononuclear cells.Haematologica · 2017Article
- Article
- Delayed Imatinib Treatment for Acute Spinal Cord Injury: Functional Recovery and Serum Biomarkers.Journal of neurotrauma · 2015Article
- Four cases of chronic myelogenous leukemia in mixed phenotype blast phase at initial presentation mimicking mixed phenotype acute leukemia with t(9;22).Annals of laboratory medicine · 2014Article
- Regulation of monocyte differentiation by specific signaling modules and associated transcription factor networks.Cellular and molecular life sciences : CMLS · 2014Review
- Investigation into the biological properties of the olive polyphenol, hydroxytyrosol: mechanistic insights by genome-wide mRNA-Seq analysis.Genes & nutrition · 2012Article
- OCT-1 function varies with cell lineage but is not influenced by BCR-ABL.Haematologica · 2011Article
- Gene set analysis exploiting the topology of a pathway.BMC systems biology · 2010Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism that is responsible for mature neutrophil overproduction in the chronic phase (CP) of chronic myeloid leukemia (CML), a neoplastic disease of hematopoietic stem cells carrying a constitutively active tyrosine kinase BCR-ABL, remains obscure. In this study, microarray analysis revealed that c-Jun, a monopoiesis-promoting transcription factor, was downregulated in CML neutrophils. BCR-ABL directly inhibited c-Jun expression, as c-Jun downregulation in primary CML neutrophils and in the CML blast cell lines, KCL22 and K562, was reversed by the tyrosine kinase inhibitor imatinib. We established a myeloid differentiation model in KCL22 cells using zinc-inducible CCAAT/enhancer-binding protein (C/EBP)alpha (KCL22/alpha). Myeloid differentiation was observed in C/EBP-induced KCL22/alpha cells. Imatinib-induced c-Jun upregulation promoted the monocytic differentiation of KCL22/alpha cells. c-Jun knockdown in KCL22/alpha cells by a short interfering RNA redirected their differentiation from the monocytic to the neutrophilic lineage, even after imatinib treatment. A blockade of PI3K-Akt signaling with an Akt inhibitor upregulated c-Jun and induced the monocytic differentiation of KCL22, K562, and C/EBP-induced KCL22/alpha cells. Thus, BCR-ABL downregulates c-Jun expression by activating the PI3K-Akt pathway during CML-CP, thereby allowing C/EBPs to promote neutrophil differentiation.
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