Key result
Low-dose aspirin exerts anticancer activity by irreversibly inhibiting platelet cyclooxygenase-1, blocking the procarcinogenic action of platelets.
Why the study?
Low-dose aspirin has emerged as an anticancer drug, and whether platelets and irreversible inhibition of platelet cyclooxygenase-1 are the primary targets remains an open question.
Does low-dose aspirin exert anticancer activity by irreversibly inhibiting platelet cyclooxygenase-1?
Does low-dose aspirin exert anticancer activity by irreversibly inhibiting platelet cyclooxygenase-1?
Low-dose aspirin may exert its anticancer and anti-metastatic effects primarily through the irreversible inhibition of platelet cyclooxygenase-1.
Supports further study of platelet-targeted aspirin in oncology; leaves open clinical adoption pending higher-level trials.
Aspirin, when administered at low doses, has emerged as a powerful anticancer drug due to both chemopreventive activity against many forms of cancer and its ability to block metastases when administered postdiagnosis. Platelets, which are often elevated in circulation during the latter stages of cancer, are known to promote epithelial-mesenchymal transition, cancer cell growth, survival in circulation, and angiogenesis at sites of metastases. Low-dose aspirin has been demonstrated to block this procarcinogenic action of platelets. In this article, we present evidence that aspirin's unique ability to irreversibly inhibit platelet cyclooxygenase-1 is a key mechanism by which aspirin exerts anticancer activity.
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Lichtenberger et al. (2019) conducted a review in Cancer. Aspirin was evaluated. Low-dose aspirin exerts anticancer activity by irreversibly inhibiting platelet cyclooxygenase-1, blocking the procarcinogenic action of platelets.
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