Peer-reviewed veterinary case report
Glutaminase blocker CB-839 tested on canine large-cell lymphoma cells
By Kosei Sakai et al.·Published in Veterinary Medicine and Science·2025·Laboratory of Small Animal Internal Medicine 1, School of Veterinary Medicine Kitasato University Aomori Japan, GB·View original on DOAJ →
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Original publication title: Glutaminase Expression in Canine Large‐Cell Alimentary Lymphoma Cells and Effects of Glutaminase Inhibition by CB‐839
- Species:
- dog
Plain-English summary
A study looked at how a drug called CB-839, which inhibits glutaminase, affects large-cell lymphoma in dogs. Researchers found that glutaminase levels were higher in cancer cells compared to healthy cells, and when they treated the cancer cells with CB-839, it slowed down their growth and even caused some to die. The treatment worked better on certain cell lines than others, suggesting that glutaminase is important for the cancer's survival. This research points to the potential of using glutaminase inhibitors like CB-839 as a treatment option for dogs with this type of lymphoma.
People also search for: dog lymphoma treatment · canine cancer drugs · CB-839 for dogs · large-cell lymphoma in dogs · glutaminase inhibitor for dogs
Abstract
ABSTRACT Glutamine metabolism plays a crucial role in tumour progression, making glutaminase a promising therapeutic target in various human cancers. However, its role in canine large‐cell alimentary lymphoma (AL) remains unclear. This study investigated glutaminase expression and the effects of a glutaminase inhibitor (CB‐839) on canine large‐cell AL cell lines. Western blotting analysed glutaminase expression in three canine large‐cell AL cell lines (CLC, Ema and Nody‐1) and peripheral blood mononuclear cells (PBMCs) isolated from eight clinically healthy dogs. Cell viability was determined in each cell line after treatment with varying concentrations (0–10 µM) of CB‐839. Flow cytometry was used to analyse the cell cycle and assess annexin assays in each cell line following treatment with 1 µM of CB‐839 or a vehicle control. Additionally, metabolome analysis was performed in Nody‐1 cells after treatment with 1 µM of CB‐839 or a vehicle control. Glutaminase expression was significantly higher in cell lines than in PBMCs. CB‐839 suppressed cell proliferation in a dose‐dependent manner, with CLC and Nody‐1 cells exhibiting greater susceptibility than Ema cells. Flow cytometric analysis revealed that CB‐839 induced G0/G1 phase arrest and apoptosis in susceptible cell lines. Metabolomic analysis revealed that CB‐839 led to glutamine accumulation and depletion of key tricarboxylic acid cycle intermediates in Nody‐1 cells. These findings indicate that glutamine metabolism is upregulated in canine large‐cell AL and plays a crucial role in tumour cell growth and survival. Inhibiting glutaminase could serve as a promising therapeutic strategy for this disease.
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Search related cases →Original publication on DOAJ: https://doi.org/10.1002/vms3.70601