ArticleNature communications2023
Systematic characterization of the HOXA9 downstream targets in MLL-r leukemia by noncoding CRISPR screens.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 7 citations in OpenAlex.
- Towards efficient perturbation for the noncoding genome.Nature communications · 2026Article
- MBNL1 hijacks a structured single-stranded distal DNA element to sustainScience advances · 2026Article
- Deciphering resistance mechanisms to auxin-inducible protein degradation in mammalian cells.The Journal of biological chemistry · 2026Article
- The hidden regulators: Non-coding RNAs in KMT2A-rearranged acute lymphoblastic leukemia.International journal of cancer · 2026Review
- Deciphering acquired resistance mechanisms to sustained auxin-inducible protein degradation in cells and mice.bioRxiv : the preprint server for biology · 2025Article
- Signature of leukemia stem cell death pattern predicts prognosis and therapeutic response of acute myeloid leukemia patients.Scientific reports · 2025Article
- Pbx3-mediated suppression of type I interferon response contributes to leukemia progression driven by MLL-AF9.Cancer gene therapy · 2025Article
- CTCF is selectively required for maintaining chromatin accessibility and gene expression in human erythropoiesis.Genome biology · 2025Article
- Induction of AML cell differentiation using HOXA9/DNA binding inhibitors as a potential therapeutic option for HOXA9-dependent AML.HemaSphere · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Accumulating evidence indicates that HOXA9 dysregulation is necessary and sufficient for leukemic transformation and maintenance. However, it remains largely unknown how HOXA9, as a homeobox transcriptional factor, binds to noncoding regulatory sequences and controls the downstream genes. Here, we conduct dropout CRISPR screens against 229 HOXA9-bound peaks identified by ChIP-seq. Integrative data analysis identifies reproducible noncoding hits, including those located in the distal enhancer of FLT3 and intron of CDK6. The Cas9-editing and dCas9-KRAB silencing of the HOXA9-bound sites significantly reduce corresponding gene transcription and impair cell proliferation in vitro, and in vivo by transplantation into NSG female mice. In addition, RNA-seq, Q-PCR analysis, chromatin accessibility change, and chromatin conformation evaluation uncover the noncoding regulation mechanism of HOXA9 and its functional downstream genes. In summary, our work improves our understanding of how HOXA9-associated transcription programs reconstruct the regulatory network specifying MLL-r dependency.
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Registered trials
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