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Nilotinib: Disrupting the MYC-MAX Heterocomplex.

Kamilla Shah1, Maham Ansari1, Samina Saeed1

  • 1Department of Biotechnology, Faculty of Life Sciences & Informatics, Balochistan University of Information Technology, Engineering and Management Sciences (BUITEMS), Quetta, Pakistan.

Bioinformatics and Biology Insights
|July 31, 2024
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Summary

Researchers repurposed the tyrosine kinase inhibitor nilotinib to target the MYC-MAX cancer-promoting interaction. This drug stabilizes MYC, inhibiting cancer-driving gene expression and offering a new therapeutic avenue for aggressive cancers.

Keywords:
Anti-cancer drugsMYC oncogeneactivity-based (QSAR) virtual screeningdifferential gene expressiondrug repositioning/repurposingmolecular dynamics simulationnilotinibstructure-based virtual screening

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Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • MYC is a critical transcription factor for cellular homeostasis; its dysregulation drives aggressive cancers.
  • The MYC-MAX heterodimer promotes oncogenesis, but targeting this interaction with small molecules has been challenging.
  • MYC's 'undruggable' status stems from its unstable protein structure, necessitating novel therapeutic strategies.

Purpose of the Study:

  • To explore drug repurposing for inhibiting the c-MYC-MAX interaction using computer-aided methods.
  • To identify existing drugs that can stabilize MYC and disrupt its oncogenic function.
  • To evaluate nilotinib as a potential therapeutic agent against MYC-driven cancers.

Main Methods:

  • Utilized computer-aided drug design, including virtual screening of the DrugBank library.
  • Employed structure-based (AutoDock Vina, Glide) and activity-based (QSPR models) screening approaches.
  • Performed molecular dynamic simulations and gene expression analysis to validate drug-target interactions.

Main Results:

  • Identified a druggable site on c-MYC and screened DrugBank compounds, focusing on the top 2% of hits.
  • Nilotinib, a tyrosine kinase inhibitor (TKI), emerged as a promising candidate, stabilizing MYC and its interaction with MAX.
  • Nilotinib induced a gene expression profile, with half of the genes being c-MYC-responsive, suggesting targeted inhibition.

Conclusions:

  • Nilotinib demonstrates potential as a therapeutic agent for MYC-driven cancers by stabilizing the MYC protein.
  • This study provides a foundation for further in vitro and in vivo validation of nilotinib's efficacy.
  • Drug repurposing offers a viable strategy to target previously 'undruggable' oncoproteins like MYC.