Abstract Number: PB1389
Meeting: ISTH 2020 Congress
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.
To cite this abstract in AMA style:Wang J-, Chen C-, Chen W-, Li J-, Lin S-, Wang Y-. The Effect of Aspirin in Tumor Growth of Obese Mice Involving Inhibition of Metabolism [abstract]. Res Pract Thromb Haemost. 2020; 4 (Suppl 1). https://abstracts.isth.org/abstract/the-effect-of-aspirin-in-tumor-growth-of-obese-mice-involving-inhibition-of-metabolism/. Accessed January 21, 2022.
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