ArticleOncogene2003
The fusion protein AML1-ETO in acute myeloid leukemia with translocation t(8;21) induces c-jun protein expression via the proximal AP-1 site of the c-jun promoter in an indirect, JNK-dependent manner.
Article in Oncogene, 2003. 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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Who cites it
20 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- Upregulation of ALDH1 as an adaptive epigenetic response to anthracyclines in acute myeloid leukemia.HemaSphere · 2025Article
- Leukemic stem cells activate lineage inappropriate signalling pathways to promote their growth.Nature communications · 2024Article
- A CIBERSORTx-based immune cell scoring system could independently predict the prognosis of patients with myelodysplastic syndromes.Blood advances · 2021Article
- TNF-α signaling regulates RUNX1 function in endothelial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Review
- The Oncogenic Transcription Factor RUNX1/ETO Corrupts Cell Cycle Regulation to Drive Leukemic Transformation.Cancer cell · 2018Article
- Synergistic suppression of t(8;21)-positive leukemia cell growth by combining oridonin and MAPK1/ERK2 inhibitors.Oncotarget · 2017Article
- JUN is a key transcriptional regulator of the unfolded protein response in acute myeloid leukemia.Leukemia · 2017Article
- Suppression of RUNX1/ETO oncogenic activity by a small molecule inhibitor of tetramerization.Haematologica · 2017Article
- Elevated PIN1 expression by C/EBPalpha-p30 blocks C/EBPalpha-induced granulocytic differentiation through c-Jun in AML.Leukemia · 2010Article
- Complementing mutations in core binding factor leukemias: from mouse models to clinical applications.Oncogene · 2008Review
- Article
- The p21Waf1 pathway is involved in blocking leukemogenesis by the t(8;21) fusion protein AML1-ETO.Blood · 2007Article
- Commonly dysregulated genes in murine APL cells.Blood · 2007Article
- Runx1/AML1 in normal and abnormal hematopoiesis.International journal of hematology · 2005Review
- AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: implication in stepwise leukemogenesis and response to Gleevec.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- The 8;21 translocation in leukemogenesis.Oncogene · 2004Review
- Effects of the leukemia-associated AML1-ETO protein on hematopoietic stem and progenitor cells.Oncogene · 2004Review
- Elevated c-Jun expression in acute myeloid leukemias inhibits C/EBPalpha DNA binding via leucine zipper domain interaction.Oncogene · 2003Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Overexpression of proto-oncogene c-jun and constitutive activation of the Jun N-terminal kinase (JNK) signaling pathway have been implicated in the leukemic transformation process. However, c-jun expression and the role of the JNK signaling pathway have not been investigated in primary acute myeloid leukemia (AML) cells with frequently observed balanced rearrangements such as t(8;21). In the present study, we report elevated c-jun mRNA expression in AML patient bone marrow cells with t(8;21), t(15;17) or inv(16), and a high correlation in mRNA expression levels of AML1-ETO and c-jun within t(8;21)-positive AML patient cells. In myeloid U937 cells, c-jun mRNA and protein expression increase upon inducible expression of AML1-ETO. AML1-ETO transactivates the human c-jun promoter through the proximal activator protein (AP-1) site by activating the JNK pathway. Overexpression of JNK-inhibitor JIP-1 and chemical JNK inhibitors reduce the transactivation capacity of AML1-ETO on the c-jun promoter and the proapoptotic function of AML1-ETO in U937 cells. An autocrine mechanism involving granulocyte-colony stimulating factor (G-CSF) and G-CSF receptor (G-CSF-R) might participate in AML1-ETO mediated JNK-signaling, because AML1-ETO induces G-CSF and G-CSF-R expression, and G-CSF-R-neutralizing antibodies reduce AML1-ETO-induced JNK phosphorylation. These data suggest a model in which AML1-ETO induces proto-oncogene c-jun expression via the proximal AP-1 site of the c-jun promoter in a JNK-dependent manner.
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