Key result
Ticagrelor reduces tumor metastasis in vivo by inducing platelet apoptosis and inhibiting carcinoma cell proliferation.
Why the study?
Platelet activation facilitates tumor cell survival and dissemination, making platelet inhibition or blocking platelet-tumor cell interactions a strategy to suppress tumor progression.
Does ticagrelor reduce tumor metastasis and cell proliferation in preclinical models?
Does ticagrelor reduce tumor metastasis and cell proliferation in preclinical models?
Answers are grounded in this paper and cite their sources.
Ticagrelor demonstrates potential anti-tumor properties by inhibiting tumor cell proliferation and metastasis and promoting platelet apoptosis in preclinical models.
Tumor cells can activate platelets, which in turn facilitate tumor cell survival and dissemination. Platelets inhibition or blocking platelet-tumor cell interactions has become a strategy to suppress tumor progression. In this study, we investigated the effect of ticagrelor, a new antiplatelet drug, on tumor cell proliferation and metastasis. Our results show that ticagrelor not only inhibits the proliferation, migration, and invasion of B16F10 and Lewis lung carcinoma cells but also induces platelet apoptosis. In addition, we find that apoptosis of the platelet cells is dose dependent. Further, the result of in-vivo experiments proved that ticagrelor treatment decreased the tumor metastasis. The results of this study demonstrate that ticagrelor may be a potential anti-tumor agent for tumor metastasis.
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Meng et al. (2020) studied Tumor metastasis. Ticagrelor was evaluated on Tumor cell proliferation, migration, invasion, platelet apoptosis, and tumor metastasis. Ticagrelor inhibited the proliferation, migration, and invasion of B16F10 and Lewis lung carcinoma cells, induced dose-dependent platelet apoptosis, and decreased tumor metastasis in vivo.
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