ArticleJournal of hematology & oncology2017
The stem cell factor SALL4 is an essential transcriptional regulator in mixed lineage leukemia-rearranged leukemogenesis.
Article in Journal of hematology & oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Identification and validation of an autophagy-related signature for predicting survival in lower-grade glioma.Bioengineered · 2021Trial
- A function of Spalt proteins in heterochromatin organization and maintenance of genomic DNA integrity.Development (Cambridge, England) · 2025Article
- Thalidomide-induced limb malformations: an update and reevaluation.Archives of toxicology · 2025Review
- SALL4 mediates SHP2 inhibition in myocardial fibroblasts through the DOT1L/H3K79me2 signaling pathway to promote the progression of myocardial infarction.Scientific reports · 2024Article
- HOXC12 promotes the invasion and migration of gastric cancer cells by upregulating SALL4 and activating Wnt/β-catenin signaling pathway.Discover oncology · 2024Article
- Cancer stem cells: advances in knowledge and implications for cancer therapy.Signal transduction and targeted therapy · 2024Review
- Acute lymphoblastic leukemia in children and SALL4 and BMI-1 gene expression.Pediatric research · 2023Article
- Molecular basis of RNA-binding and autoregulation by the cancer-associated splicing factor RBM39.Nature communications · 2023Article
- SALL4 promotes angiogenesis in gastric cancer by regulating VEGF expression and targeting SALL4/VEGF pathway inhibits cancer progression.Cancer cell international · 2023Article
- SALL4 correlates with proliferation, metastasis, and poor prognosis in prostate cancer by affecting MAPK pathway.Cancer medicine · 2023Article
- The new advance of SALL4 in cancer: Function, regulation, and implication.Journal of clinical laboratory analysis · 2023Review
- DNA methyltransferase-1 in acute myeloid leukaemia: beyond the maintenance of DNA methylation.Annals of medicine · 2022Review
- Cyclin D1 mediated by the nuclear translocation of nuclear factor kappa B exerts an oncogenic role in lung cancer.Bioengineered · 2022Article
- SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022Review
- Construction and validation of an immunity-related prognostic signature for breast cancer.Aging · 2020Article
- Overexpression of Sal-like protein 4 in head and neck cancer: epigenetic effects and clinical correlations.Cellular oncology (Dordrecht, Netherlands) · 2020Article
- Expression and clinical value of SALL4 in renal cell carcinomas.Molecular medicine reports · 2020Article
- Crosstalk between MEIS1 and markers of different cell signaling pathways in esophageal squamous cell carcinoma.Molecular biology reports · 2020Article
- 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
- Thalidomide Inhibits Human iPSC Mesendoderm Differentiation by Modulating CRBN-dependent Degradation of SALL4.Scientific reports · 2020Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe stem cell factor spalt-like transcription factor 4 (SALL4) plays important roles in normal hematopoiesis and also in leukemogenesis. We previously reported that SALL4 exerts its effect by recruiting important epigenetic factors such as DNA methyltransferases DNMT1 and lysine-specific demethylase 1 (LSD1/KDM1A). Both of these proteins are critically involved in mixed lineage leukemia (MLL)-rearranged (MLL-r) leukemia, which has a very poor clinical prognosis. Recently, SALL4 has been further linked to the functions of MLL and its target gene homeobox A9 (HOXA9). However, it remains unclear whether SALL4 is indeed a key player in MLL-r leukemia pathogenesis.
methodsUsing a mouse bone marrow retroviral transduction/ transplantation approach combined with tamoxifen-inducible, CreER
resultsIn vitro and in vivo studies revealed that SALL4 expression is critically required for MLL-AF9-induced leukemic transformation and disease progression in mice. Loss of SALL4 in MLL-AF9-transformed cells induced apoptosis and cell cycle arrest at G1. ChIP-Seq assay identified that Sall4 binds to key MLL-AF9 target genes and important MLL-r or non-MLL-r leukemia-related genes. ChIP-PCR assays indicated that SALL4 affects the levels of the histone modification markers H3K79me2/3 and H3K4me3 at MLL-AF9 target gene promoters by physically interacting with DOT1-like histone H3K79 methyltransferase (DOT1l) and LSD1/KDM1A, and thereby regulates transcript expression. Surprisingly, normal Sall4
conclusionsOur findings indicate that SALL4 critically contributes to MLL-AF9-induced leukemia, unraveling the underlying transcriptional and epigenetic mechanisms in this disease and suggesting that selectively targeting the SALL4 pathway may be a promising approach for managing human MLL-r leukemia.
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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.