ArticleBlood advances2022
BCL11A promotes myeloid leukemogenesis by repressing PU.1 target genes.
Article in Blood advances, 2022. 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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20 citing papers in PubMed, 34 citations in OpenAlex.
- Autoinhibitory feedback preserves intestinal stem cell maintenance and fate commitment.The EMBO journal · 2026Article
- Proteomics landscape of early T-cell precursor acute lymphoblastic leukemia reveals deficient oxidative phosphorylation signatures.Cell reports. Medicine · 2026Article
- Integrated analysis of the blood metallome and DNA methylation, gene expression, and protein levels of immune-associated genes in residents from mining region.Environmental geochemistry and health · 2026Article
- The transcription factor Bcl11a is essential for B-1a cell maintenance during aging.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Transcriptional and epigenetic rewiring by the NUP98::KDM5A fusion oncoprotein directly activates CDK12.Nature communications · 2025Article
- Solution structure of the Z0 domain from transcription repressor BCL11A sheds light on the sequence properties of protein-binding zinc fingers.Protein science : a publication of the Protein Society · 2025Article
- Lactylation modulation identifies key biomarkers and therapeutic targets in KMT2A-rearranged AML.Scientific reports · 2025Article
- Review
- Rapid increase of C/EBPα p42 induces growth arrest of acute myeloid leukemia (AML) cells by Cop1 deletion in Trib1-expressing AML.Leukemia · 2024Article
- Transcriptional regulators of fetal hemoglobin.Hematology, transfusion and cell therapy · 2024Review
- RUNX1 interacts with lncRNA SMANTIS to regulate monocytic cell functions.Communications biology · 2024Article
- Dysregulated innate immune signaling cooperates with RUNX1 mutations to transform an MDS-like disease to AML.iScience · 2024Article
- miR-365-3p mediates BCL11A and SOX6 erythroid-specific coregulation: A new player in HbF activation.Molecular therapy. Nucleic acids · 2023Article
- The transcription factor HIF2α partakes in the differentiation block of acute myeloid leukemia.EMBO molecular medicine · 2023Article
- Article
- ThPOK is a critical multifaceted regulator of myeloid lineage development.Nature immunology · 2023Article
- BCL7A is silenced by hypermethylation to promote acute myeloid leukemia.Biomarker research · 2023Article
- SWI/SNF complexes in hematological malignancies: biological implications and therapeutic opportunities.Molecular cancer · 2023Review
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- Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcriptional repressor BCL11A is involved in hematological malignancies, B-cell development, and fetal-to-adult hemoglobin switching. However, the molecular mechanism by which it promotes the development of myeloid leukemia remains largely unknown. We find that Bcl11a cooperates with the pseudokinase Trib1 in the development of acute myeloid leukemia (AML). Bcl11a promotes the proliferation and engraftment of Trib1-expressing AML cells in vitro and in vivo. Chromatin immunoprecipitation sequencing analysis showed that, upon DNA binding, Bcl11a is significantly associated with PU.1, an inducer of myeloid differentiation, and that Bcl11a represses several PU.1 target genes, such as Asb2, Clec5a, and Fcgr3. Asb2, as a Bcl11a target gene that modulates cytoskeleton and cell-cell interaction, plays a key role in Bcl11a-induced malignant progression. The repression of PU.1 target genes by Bcl11a is achieved by sequence-specific DNA-binding activity and recruitment of corepressors by Bcl11a. Suppression of the corepressor components HDAC and LSD1 reverses the repressive activity. Moreover, treatment of AML cells with the HDAC inhibitor pracinostat and the LSD1 inhibitor GSK2879552 resulted in growth inhibition in vitro and in vivo. High BCL11A expression is associated with worse prognosis in humans with AML. Blocking of BCL11A expression upregulates the expression of PU.1 target genes and inhibits the growth of HL-60 cells and their engraftment to the bone marrow, suggesting that BCL11A is involved in human myeloid malignancies via the suppression of PU.1 transcriptional activity.
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