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Beyond Cell Cycle Control: CDKN2A Loss Orchestrates NAD+ Metabolic Plasticity and NAMPT Inhibitor Sensitivity in

Swati Dubey1, Guanqiao Yu1, Ryana Aboul-Hosn1

  • 1Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA 90095, USA.

Biorxiv : the Preprint Server for Biology
|January 23, 2026
PubMed

Insights

Loss of the CDKN2A gene in glioblastoma creates metabolic vulnerabilities linked to NAD+ homeostasis. This discovery suggests new therapeutic strategies targeting NAD+ metabolism beyond broad inhibition approaches.

Area of Science:

  • Oncology
  • Metabolic pathways
  • Cancer genetics

Background:

  • The CDKN2A gene is known to regulate the cell cycle via the p16-Cdk4-Rb pathway.
  • CDKN2A loss is a common event in glioblastoma, a highly aggressive brain tumor.

Purpose of the Study:

  • To investigate the metabolic consequences of CDKN2A loss in glioblastoma.
  • To identify novel therapeutic targets based on altered metabolic pathways in CDKN2A-deleted glioblastoma.

Main Methods:

  • Analysis of gene expression and metabolic profiles in glioblastoma samples.
  • Investigating the role of NAD+ homeostasis in the context of CDKN2A loss.

Main Results:

  • CDKN2A deletion leads to significant alterations in NAD+ homeostasis.
  • This metabolic dysregulation presents a vulnerability in CDKN2A-deleted glioblastoma cells.
  • A novel link between cell cycle deregulation and metabolic pathways was identified.

Conclusions:

  • CDKN2A loss in glioblastoma induces metabolic vulnerabilities related to NAD+ homeostasis.
  • Targeting NAD+ metabolism offers a promising therapeutic avenue for CDKN2A-deleted glioblastoma.
  • This research opens new avenues for precision medicine in glioblastoma treatment.
Keywords:
CDKN2AGlioblastomaNAD metabolismNAMPTSLC25A51

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