Unknown

Dataset Information

0

P-selectin-mediated platelet adhesion promotes tumor growth.


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 ?3 cytoplasmic tail. This activates ?IIb?3 and recruits platelets into tumors. Platelet infiltration into solid tumors occurs through a P-selectin-dependent mechanism.

SUBMITTER: Qi C 

PROVIDER: S-EPMC4466636 | biostudies-literature | 2015 Mar

REPOSITORIES: biostudies-literature

altmetric image

Publications


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 αIIbβ3 and recruits platelets into tumors. Platelet infiltr  ...[more]

Similar Datasets

| S-EPMC3954694 | biostudies-literature
| S-EPMC4440258 | biostudies-literature
| S-EPMC3493105 | biostudies-literature
| S-EPMC3047470 | biostudies-literature
| S-EPMC6298231 | biostudies-literature
| S-EPMC1853301 | biostudies-literature
| S-EPMC2947284 | biostudies-literature
| S-EPMC6811810 | biostudies-literature
| S-EPMC2825940 | biostudies-literature
| S-EPMC5399174 | biostudies-literature