Abstract
Blood platelets foster carcinogenesis. We found that platelets are accumulated in human tumors. P-selectin deficiency and soluble P-selectin abolish platelet deposition within tumors, decreasing secretion of vascular endothelial growth factor and angiogenesis, thereby suppressing tumor growth. Binding of the P-selectin cytoplasmic tail to talin1 triggers the talin1 N-terminal head to interact with the β3 cytoplasmic tail. This activates aIIbβ3 and recruits platelets into tumors. Platelet infiltration into solid tumors occurs through a P-selectin-dependent mechanism.
Original language | English (US) |
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Pages (from-to) | 6584-6596 |
Number of pages | 13 |
Journal | Oncotarget |
Volume | 6 |
Issue number | 9 |
DOIs | |
State | Published - 2015 |
Keywords
- P-selectin
- Platelets
- Talin1
- Tumor growth
- aIIbβ3
ASJC Scopus subject areas
- Oncology