ArticleBlood2013
Targeting transcription factor SALL4 in acute myeloid leukemia by interrupting its interaction with an epigenetic complex.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- SALL4 and microRNA: The Role of Let-7.Genes · 2021Pooled it
- Aberrant expression of SALL4 in acute B cell lymphoblastic leukemia: mechanism, function, and implication for a potential novel therapeutic target.Experimental hematology · 2014Trial
- SALL4-targeted therapeutic peptide PEN-FFW suppresses PD-L1 and enhances CD8⁺ T cell cytotoxicity via regulating PI3K/AKT signaling in breast cancer.Immunologic research · 2026Article
- SALL4 is a CRL3Cell death and differentiation · 2024Article
- The new advance of SALL4 in cancer: Function, regulation, and implication.Journal of clinical laboratory analysis · 2023Review
- Review
- Demethylation and Up-Regulation of an Oncogene after Hypomethylating Therapy.The New England journal of medicine · 2022Article
- SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022Review
- SALL Proteins; Common and Antagonistic Roles in Cancer.Cancers · 2021Review
- Epigenetic control of melanoma cell invasiveness by the stem cell factor SALL4.Nature communications · 2021Article
- Ush regulates hemocyte-specific gene expression, fatty acid metabolism and cell cycle progression and cooperates with dNuRD to orchestrate hematopoiesis.PLoS genetics · 2021Article
- Interplay between cofactors and transcription factors in hematopoiesis and hematological malignancies.Signal transduction and targeted therapy · 2021Review
- Zinc Finger Protein SALL4 Functions through an AT-Rich Motif to Regulate Gene Expression.Cell reports · 2021Article
- The Interplay between Transcription Factor SALL4 and Histone Modifiers in Hematopoietic Stem and Progenitor Cells.Journal of cellular immunology · 2021Article
- Expression and clinical value of SALL4 in renal cell carcinomas.Molecular medicine reports · 2020Article
- Article
- VHL mutation-mediated SALL4 overexpression promotes tumorigenesis and vascularization of clear cell renal cell carcinoma via Akt/GSK-3β signaling.Journal of experimental & clinical cancer research : CR · 2020Article
- The Methyl-CpG-Binding Domain 2 and 3 Proteins and Formation of the Nucleosome Remodeling and Deacetylase Complex.Journal of molecular biology · 2020Review
- Spalt-Like Protein 4 (SALL4) Promotes Angiogenesis by Activating Vascular Endothelial Growth Factor A (VEGFA) Signaling.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- A low-molecular-weight compound exerts anticancer activity against breast and lung cancers by disrupting EGFR/Eps8 complex formation.Journal of experimental & clinical cancer research : CR · 2019Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
An exciting recent approach to targeting transcription factors in cancer is to block formation of oncogenic complexes. We investigated whether interfering with the interaction of the transcription factor SALL4, which is critical for leukemic cell survival, and its epigenetic partner complex represents a novel therapeutic approach. The mechanism of SALL4 in promoting leukemogenesis is at least in part mediated by its repression of the tumor suppressor phosphatase and tensin homolog deleted on chromosome 10 (PTEN) through its interaction with a histone deacetylase (HDAC) complex. In this study, we demonstrate that a peptide can compete with SALL4 in interacting with the HDAC complex and reverse its effect on PTEN repression. Treating SALL4-expressing malignant cells with this peptide leads to cell death that can be rescued by a PTEN inhibitor. The antileukemic effect of this peptide can be confirmed on primary human leukemia cells in culture and in vivo, and is identical to that of down-regulation of SALL4 in these cells using an RNAi approach. In summary, our results demonstrate a novel peptide that can block the specific interaction between SALL4 and its epigenetic HDAC complex in regulating its target gene, PTEN. Furthermore, targeting SALL4 with this approach could be an innovative approach in treating leukemia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.