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ZNF224 is a transcriptional repressor of AXL in chronic myeloid leukemia cells

Gaetano Sodaro1, Giancarlo Blasio1, Federica Fiorentino1

  • 1Department of Molecular Medicine and Medical Biotechnology, University of Naples Federico II, Naples, 80131, Italy.

Biochimie
|September 4, 2018
PubMed

Insights

Zinc finger protein 224 (ZNF224) suppresses tumors in chronic myelogenous leukemia by repressing Axl. Overexpressing ZNF224 can restore imatinib sensitivity in resistant cells by reducing Axl levels.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Chronic myelogenous leukemia (CML) is a hematologic malignancy.
  • ZNF224 is a transcription factor with known tumor-suppressive functions in CML.
  • Axl receptor tyrosine kinase is overexpressed in various cancers and linked to drug resistance.

Purpose of the Study:

  • To identify novel targets of ZNF224 transcriptional repression.
  • To investigate the role of ZNF224 in regulating Axl expression.
  • To explore the therapeutic potential of ZNF224 in imatinib-resistant CML.

Main Methods:

  • Luciferase reporter assays to assess transcriptional activity.
  • Western blotting to detect protein expression levels.
  • Cell culture experiments with ZNF224 overexpression in CML cell lines.

Main Results:

  • ZNF224 directly represses the expression of the Axl receptor tyrosine kinase.
  • Overexpression of ZNF224 leads to decreased Axl levels in CML cells.
  • Restoration of imatinib sensitivity was observed in resistant CML cells upon ZNF224 induction and subsequent Axl suppression.

Conclusions:

  • Axl is a novel transcriptional target of the tumor suppressor ZNF224.
  • ZNF224-mediated suppression of Axl can overcome imatinib resistance in CML.
  • ZNF224 represents a potential therapeutic strategy for imatinib-resistant CML.
Keywords:
AxlChronic myelogenous leukemiaImatinib-resistanceTranscriptionZNF224

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