ArticleOncogene2024
Suppression of super-enhancer-driven TAL1 expression by KLF4 in T-cell acute lymphoblastic leukemia.
Article in Oncogene, 2024. 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, 9 citations in OpenAlex.
- Super-Enhancer-Driven SOX4/SMAD3 Mediate Membrane Remodeling by Regulating Phospholipid Metabolism to Accelerate Leukemia Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Krüppel-Like Factor 4, a Hub Gate for Cell Crosstalk in Tumor Microenvironment.Cancer medicine · 2026Review
- Zinc-Induced PKCδ-dependent Phosphorylation of MTF-1 Promotes Pulmonary Vascular Remodeling in Hypoxic Pulmonary Hypertension.International journal of biological sciences · 2026Article
- Induction of T-Cell Differentiation by KLF4 in T-Cell Acute Lymphoblastic Leukemia Cells Harboring Activating Mutation in NOTCH3.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Induction of plasmalemmal vesicle-associated protein exacerbates glomerular endothelial injury in thrombotic microangiopathy.American journal of physiology. Renal physiology · 2025Article
- Super enhancers as key drivers of gene regulatory networks in normal and malignant hematopoiesis.Frontiers in cell and developmental biology · 2025Review
- Enhancer looping protein LDB1 modulates MYB expression in T-ALL cell lines in vitro by cooperating with master transcription factors.Journal of experimental & clinical cancer research : CR · 2024Article
- Oncogenic Enhancers in Leukemia.Blood cancer discovery · 2024Review
- NUP98-BPTF promotes oncogenic transformation through PIM1 upregulation.Cancer medicine · 2024Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
TAL1 is one of the most frequently dysregulated genes in T-ALL and is overexpressed in about 50% of T-ALL cases. One of the molecular mechanisms of TAL1 overexpression is abnormal mutations in the upstream region of the TAL1 promoter that introduce binding motifs for the MYB transcription factor. MYB binding at this location creates a 5' TAL1 super-enhancer (SE), which leads to aberrant expression of TAL1 and is associated with unfavorable clinical outcomes. Although targeting TAL1 is considered to be an attractive therapeutic strategy for patients with T-ALL, direct inhibition of transcription factors is challenging. Here, we show that KLF4, a known tumor suppressor in leukemic cells, suppresses SE-driven TAL1 expression in T-ALL cells. Mechanistically, KLF4 downregulates MYB expression by directly binding to its promoter and inhibits the formation of 5' TAL1 SE. In addition, we found that APTO-253, a small molecule inducer of KLF4, exerts an anti-leukemic effect by targeting SE-driven TAL1 expression in T-ALL cells. Taken together, our results suggest that the induction of KLF4 is a promising strategy to control TAL1 expression and could be a novel treatment for T-ALL patients with a poor prognosis.
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