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Platelets prevent CTC death through several mechanisms: 1) interaction between breast cancer cells and platelets has been shown to activate the TGF- signaling pathway, which promotes metastasis and causes immunosuppression by downregulating DNAM-1 (CD226) and TACTILE (CD96) expression in NK cells [57, 72], 2) breast cancer cells can also pick up MHC class I antigens from platelets, helping them evade NK cell recognition as foreign cells, thereby limiting NK cell cytotoxicity [73], 3) platelets have been shown to cleave ligands such as NK group 2, member D from tumor cells surface, which prevents NK cell recognition and subsequent cytotoxicity [74], 4) another mechanism involves platelets binding to mucins on the surface of cancer cells through the GPIb-IX-V and GPIIb-IIIa adhesion molecules, mediated by surface integrins v3 or P-selectin on the cancer cells

Messenger RNA (mRNA) level data on the proteins in the HGF/Met pathway were extracted from the database and for the tumor and healthy tissue samples for each patient (Fig

This article aims to provide a comprehensive answer by examining its mechanism of action, experimental data, influencing factors, and typical timelines