ArticleCancer research2010
AML1/ETO proteins control POU4F1/BRN3A expression and function in t(8;21) acute myeloid leukemia.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Leukemic stem cells activate lineage inappropriate signalling pathways to promote their growth.Nature communications · 2024Article
- Identification and verification of a prognostic signature based on a miRNA-mRNA interaction pattern in colon adenocarcinoma.Frontiers in cell and developmental biology · 2023Article
- Longitudinal single-cell transcriptomics reveals distinct patterns of recurrence in acute myeloid leukemia.Molecular cancer · 2022Article
- MethReg: estimating the regulatory potential of DNA methylation in gene transcription.Nucleic acids research · 2022Article
- Expression of the type 3 InsPGut · 2019Article
- Elucidation of Novel Therapeutic Targets for Acute Myeloid Leukemias withInternational journal of molecular sciences · 2019Article
- Subtype-specific regulatory network rewiring in acute myeloid leukemia.Nature genetics · 2019Article
- Inhibition of Endosteal Vascular Niche Remodeling Rescues Hematopoietic Stem Cell Loss in AML.Cell stem cell · 2018Article
- Article
- AML1/ETO sensitizes via TRAIL acute myeloid leukemia cells to the pro-apoptotic effects of hypoxia.Cell death & disease · 2013Article
- AML1/ETO and POU4F1 synergy drives B-lymphoid gene expression typical of t(8;21) acute myeloid leukemia.Leukemia · 2012Article
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Authors and funding
6 authors at 2 institutions in 1 country.
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Abstract
A variety of genetic lesions, including chromosomal translocations, internal tandem duplications, and mutations, have been described in acute myeloid leukemia (AML). Expression profiling has shown that chromosomal translocations, in particular, are associated with distinctive patterns of gene expression. AML exhibiting the translocation t(8;21), which fuses the AML1 and ETO genes, has such a characteristic expression profile. One gene whose expression is highly correlated with the presence of the AML1/ETO fusion is POU4F1, which encodes the POU homeodomain transcription factor BRN3A. Here we show using specific siRNA in t(8;21) cells and overexpression studies in progenitor cells that AML1/ETO promotes expression of POU4F1/BRN3A. This effect requires DNA-binding function of AML1/ETO, and accordingly, AML1/ETO is bound to the POU4F1 locus in t(8;21) cells. Functionally, whereas overexpression of Brn3a in murine hematopoietic progenitor cells induces terminal myeloid differentiation, coexpression of AML1/ETO or AML1/ETO9a blocks this effect. Furthermore, Brn3a reduction by shRNA impairs AML1/ETO-induced immortalization of murine progenitors. In summary, we identify POU4F1/BRN3A as a novel potential upregulated AML1/ETO target gene whose dramatically high expression may cooperate with AML1/ETO in t(8;21) cells.
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