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Cytidine deaminase deficiency in tumor cells is associated with sensitivity to a naphthol derivative and a decrease

Hamza Mameri1,2,3,4, Géraldine Buhagiar-Labarchède1,2,3, Gaëlle Fontaine1,2,3

  • 1Institut Curie, PSL Research University, CNRS UMR 3348, 91405, Orsay, France.

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Summary

Researchers identified a new compound, X55, that selectively targets cancer cells lacking cytidine deaminase (CDA). This discovery offers a promising new avenue for developing targeted anticancer therapies, particularly for CDA-deficient tumors.

Keywords:
Cancer therapyCell metabolismCytidine deaminaseDrug sensitivityMAPT

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Area of Science:

  • Oncology
  • Biochemistry
  • Pharmacology

Background:

  • Cytidine deaminase (CDA) is downregulated in approximately 60% of cancers, presenting a potential therapeutic vulnerability.
  • Targeting CDA-deficient tumors is a critical unmet need in cancer research.

Purpose of the Study:

  • To develop a novel anticancer treatment targeting CDA-deficient tumor cells.
  • To identify a specific inhibitor that preferentially affects tumor cells with low CDA expression.

Main Methods:

  • High-throughput screening of a chemical library to identify CDA-targeting compounds.
  • Metabolomic profiling to analyze cellular changes in response to treatment.
  • Assessing the effect of the identified compound on both tumoral and non-tumoral cells.

Main Results:

  • A naphthol derivative, X55, was identified as a selective inhibitor of CDA-deficient tumor cells.
  • X55 treatment significantly disturbed the metabolome of CDA-deficient cells, impacting oncometabolite levels.
  • Downregulation of MAPT (encoding Tau) was identified as a predictive marker for X55 sensitivity.

Conclusions:

  • X55 demonstrates potential as a targeted therapy for CDA-deficient cancers.
  • CDA deficiency, mitochondrial function, and X55 response are unexpectedly linked.
  • MAPT downregulation serves as a reliable biomarker for predicting X55 efficacy.