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September 17, 2026Journal of Proteome Research

Integrated Metabolomic, Proteomic, and Phosphoproteomic Profiling Reveals Metabolic and Signaling Alterations Associated with CAMKK2 Inhibition in Gastric Cancer

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Authors

MNMohd Altaf NajarNCNikita ChoudharyNDNidhi Dwivedi

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Overview

Multiomic profiling reveals impaired nucleotide metabolism and DNA replication arrest in gastric cancer cells, highlighting CAMKK2 as a promising metabolic therapeutic target.

Key Points

  • To determine how CAMKK2 inhibition alters tumor metabolic programs and signaling networks in gastric cancer.
  • Treated gastric cancer cell models with the pharmacological CAMKK2 inhibitor STO-609.
  • Performed integrated multiomic analyses combining untargeted metabolomics, proteomics, and phosphoproteomic profiling alongside pathway analysis.
  • CAMKK2 inhibition induced G1/S phase cell cycle arrest, multinucleation, and an apparent replication-stress-like phenotype.
  • Metabolomic profiling revealed marked depletion of purine and pyrimidine intermediates alongside suppression of lipid and central carbon metabolism.
  • Proteomic and phosphoproteomic integration demonstrated coordinated downregulation of DNA replication machinery and attenuation of proliferative signaling pathways.

Cite This Study

Najar et al. (2026) studied this question.

synapsesocial.com/papers/6aabb7275f706d05830e5fc3https://doi.org/10.1021/acs.jproteome.6c00428
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