ArticleOncotarget2015
WT1-mediated repression of the proapoptotic transcription factor ZNF224 is triggered by the BCR-ABL oncogene.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- ZNF224 enhances the oncogenic function of p21 via p53 and AKT pathways in melanoma.The FEBS journal · 2025Article
- The Molecular Interplay Between p53-Mediated Ferroptosis and Non-Coding RNAs in Cancer.International journal of molecular sciences · 2025Review
- Biological relevance of ZNF224 expression in chronic lymphocytic leukemia and its implication IN NF-kB pathway regulation.Frontiers in molecular biosciences · 2022Article
- Exploring a peptide nucleic acid-based antisense approach for CD5 targeting in chronic lymphocytic leukemia.PloS one · 2022Article
- ZNF224 Protein: Multifaceted Functions Based on Its Molecular Partners.Molecules (Basel, Switzerland) · 2021Review
- Exploring the Leukemogenic Potential of GATA-1Antioxidants (Basel, Switzerland) · 2021Article
- MiR-137 Targets the 3' Untranslated Region ofCancers · 2021Article
- Oxidative Stress and ROS-Mediated Signaling in Leukemia: Novel Promising Perspectives to Eradicate Chemoresistant Cells in Myeloid Leukemia.International journal of molecular sciences · 2021Review
- KRAB-ZFP Transcriptional Regulators Acting as Oncogenes and Tumor Suppressors: An Overview.International journal of molecular sciences · 2021Review
- Article
- Role of ZNF224 in c-Myc repression and imatinib responsiveness in chronic myeloid leukemia.Oncotarget · 2018Article
- Distinct global binding patterns of the Wilms tumor gene 1 (WT1) -KTS and +KTS isoforms in leukemic cells.Haematologica · 2017Article
- The Combination ofCancer control : journal of the Moffitt Cancer CenterArticle
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Kruppel-like protein ZNF224 is a co-factor of the Wilms' tumor 1 protein, WT1. We have previously shown that ZNF224 exerts a specific proapoptotic role in chronic myelogenous leukemia (CML) K562 cells and contributes to cytosine arabinoside-induced apoptosis, by modulating WT1-dependent transcription of apoptotic genes. Here we demonstrate that ZNF224 gene expression is down-regulated both in BCR-ABL positive cell lines and in primary CML samples and is restored after imatinib and second generation tyrosine kinase inhibitors treatment. We also show that WT1, whose expression is positively regulated by BCR-ABL, represses transcription of the ZNF224 gene. Finally, we report that ZNF224 is significantly down-regulated in patients with BCR-ABL positive chronic phase-CML showing poor response or resistance to imatinib treatment as compared to high-responder patients. Taken as a whole, our data disclose a novel pathway activated by BCR-ABL that leads to inhibition of apoptosis through the ZNF224 repression. ZNF224 could thus represent a novel promising therapeutic target in CML.
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