ArticleOncotarget2018
Role of ZNF224 in c-Myc repression and imatinib responsiveness in chronic myeloid leukemia.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- ZNF224 enhances the oncogenic function of p21 via p53 and AKT pathways in melanoma.The FEBS journal · 2025Article
- Decoding the Implications of Zinc in the Development and Therapy of Leukemia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Enhanced induction of apoptosis in chronic myeloid leukemia cells through synergistic effect of telomerase inhibitor MST-312 and imatinib.Molecular biology reports · 2024Article
- siRNA-mediated downregulation of BATF3 diminished proliferation and induced apoptosis through downregulating c-Myc expression in chronic myelogenous leukemia cells.Molecular biology reports · 2024Article
- A multidisciplinary approach disclosing unexplored Aflatoxin B1 roles in severe impairment of vitamin D mechanisms of action.Cell biology and toxicology · 2023Article
- Ferritin Heavy Chain Binds Peroxiredoxin 6 and Inhibits Cell Proliferation and Migration.International journal of molecular sciences · 2022Article
- 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
- KRAB-ZFP Transcriptional Regulators Acting as Oncogenes and Tumor Suppressors: An Overview.International journal of molecular sciences · 2021Review
- Participation of MicroRNAs in the Treatment of Cancer with Phytochemicals.Molecules (Basel, Switzerland) · 2020Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor ZNF224 plays a key proapoptotic role in chronic myelogenous leukemia (CML), by modulating Wilms Tumor protein 1 (WT1) dependent apoptotic genes transcription. Recently, we demonstrated that Bcr-Abl signaling represses ZNF224 expression in Bcr-Abl positive CML cell lines and in CML patients. Interestingly, Imatinib and second-generation tyrosine kinase inhibitors specifically increase ZNF224 expression. On the other hand, Bcr-Abl positively modulates, via JAK2 activation, the expression of the c-Myc oncogene, which is required for Bcr-Abl oncogenic transformation in CML. Consequently, JAK2 inhibitors represent promising molecular therapeutic tools in CML. In this work, we demonstrate that ZNF224 is a novel transcriptional repressor of c-Myc in CML. We also show that ZNF224 induction by Imatinib and AG490, a specific JAK2 inhibitor, is responsible for the transcriptional repression of c-MYC, thus highlighting the crucial role of the ZNF224/c-Myc axis in Imatinib responsiveness. Interestingly, we also report that ZNF224 is induced by AG490 in Imatinib-resistant CML cells, leading to c-Myc repression and apoptosis induction. These findings suggest that the development of molecular tools able to induce ZNF224 expression could provide promising means to bypass Imatinib resistance in CML.
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