Background: Aspirin is a widely used antiplatelet drug. Beyond its cardiovascular and cerebrovascular effects, epidemiological, clinical, and experimental evidence has shown that aspirin plays certain roles with regards to anticancer.

Aims: This study was conducted to identify any metabolic alterations in obese mice and to also investigate the anticancer effects of aspirin on obesity-driven cancer malignancy, by taking advantage of the syngeneic tumor model.

Methods: Using a syngeneic tumor model involving Lewis Lung Carcinoma (LLC) cells and C57BL/6 mice fed with a high fat diet, obesity was found to be associated with dysregulated glucose and glutamine metabolism, inflammation, along with platelet activation and the promotion of tumor growth.

Results: Tumor-bearing lowered glucose levels while moderately increasing inflammation, platelet activation, and glutamine levels. The antiplatelet drug aspirin, mitigated tumor growth in obese mice, paralleled by a decrease in systemic glucose, insulin, inflammation, platelet activation, glutamine and tumor expression of cell proliferation, aerobic glycolysis, glutaminolysis, platelets, and leukocyte molecules.

Conclusions: The anticancer effects of the antiplatelet drug aspirin are multifactorial. Glucose and glutamine metabolism are proposed targets for the anticancer effects of aspirin.

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ISTH Congress Abstracts - https://abstracts.isth.org/abstract/the-effect-of-aspirin-in-tumor-growth-of-obese-mice-involving-inhibition-of-metabolism/