ArticleMolecular cancer2014
RNAi-mediated silencing of MLL-AF9 reveals leukemia-associated downstream targets and processes.
Article in Molecular cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- The Fanconi anemia pathway restrains MLL-rearranged leukemogenesis through suppressing non-homologous end joining-mediated genomic instability.Nature communications · 2026Article
- chromIDEAS reveals epigenetic dynamics via multi-dimensional clustering of chromatin states.Nucleic acids research · 2026Article
- A novel human acute myeloid leukemia cell line SDEY-AML1 with KMT2A: MLLT3, IKZF1: EVX1 fusions exhibits high tumorigenicity in NSG mice.Scientific reports · 2026Article
- Screening and experimental study of potential biomarkers for ulcerative colitis based on weighted gene co-expression network analysis and machine learning.Journal of translational medicine · 2025Article
- Identification of transcription factors dictating blood cell development using a bidirectional transcription network-based computational framework.Scientific reports · 2022Article
- A proteolysis-targeting chimera molecule selectively degrades ENL and inhibits malignant gene expression and tumor growth.Journal of hematology & oncology · 2022Article
- ZNF521 Enhances MLL-AF9-Dependent Hematopoietic Stem Cell Transformation in Acute Myeloid Leukemias by Altering the Gene Expression Landscape.International journal of molecular sciences · 2021Article
- Article
- Small-molecule inhibitor of AF9/ENL-DOT1L/AF4/AFF4 interactions suppresses malignant gene expression and tumor growth.Theranostics · 2021Article
- Characterization of Copy Number Variations in Oral Cavity Squamous Cell Carcinoma Reveals a Novel Role for MLLT3 in Cell Invasiveness.The oncologist · 2019Article
- Article
- Serotonin receptor type 1B constitutes a therapeutic target for MDS and CMML.Scientific reports · 2018Article
- CRISPR Screen Reveals that EHEC's T3SS and Shiga Toxin Rely on Shared Host Factors for Infection.mBio · 2018Article
- RNA interference efficiently targets human leukemia driven by a fusion oncogene in vivo.Leukemia · 2018Article
- Article
- ZNF521 sustains the differentiation block in MLL-rearranged acute myeloid leukemia.Oncotarget · 2017Article
- miRNAs in acute myeloid leukemia.Oncotarget · 2017Review
- MLLT3 promotes proliferation of osteosarcoma cells by regulating JNK signaling.International journal of clinical and experimental pathology · 2017Article
- Gene and virotherapy for hematological malignancies.International journal of hematology · 2016Review
- The leukemogenic fusion gene MLL-AF9 alters microRNA expression pattern and inhibits monoblastic differentiation via miR-511 repression.Journal of experimental & clinical cancer research : CR · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe translocation t(9;11)(p22;q23) leading to the leukemogenic fusion gene MLL-AF9 is a frequent translocation in infant acute myeloid leukemia (AML). This study aimed to identify genes and molecular processes downstream of MLL-AF9 (alias MLL-MLLT3) which could assist to develop new targeted therapies for such leukemia with unfavorable prognosis.
methodsIn the AML cell line THP1 which harbors this t(9;11) translocation, endogenous MLL-AF9 was silenced via siRNA while ensuring specificity of the knockdown and its efficiency on functional protein level.
resultsThe differential gene expression profile was validated for leukemia-association by gene set enrichment analysis of published gene sets from patient studies and MLL-AF9 overexpression studies and revealed 425 differentially expressed genes. Gene ontology analysis was consistent with a more differentiated state of MLL-AF9 depleted cells, with involvement of a wide range of downstream transcriptional regulators and with defined functional processes such as ribosomal biogenesis, chaperone binding, calcium homeostasis and estrogen response. We prioritized 41 gene products as candidate targets including several novel and potentially druggable effectors of MLL-AF9 (AHR, ATP2B2, DRD5, HIPK2, PARP8, ROR2 and TAS1R3). Applying the antagonist SCH39166 against the dopamine receptor DRD5 resulted in reduced leukemic cell characteristics of THP1 cells.
conclusionBesides potential new therapeutic targets, the described transcription profile shaped by MLL-AF9 provides an information source into the molecular processes altered in MLL aberrant leukemia.
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