P-selectin-mediated platelet adhesion promotes tumor growth

نویسندگان

  • Cuiling Qi
  • Bo Wei
  • Weijie Zhou
  • Yang Yang
  • Bin Li
  • Simei Guo
  • Jialin Li
  • Jie Ye
  • Jiangchao Li
  • Qianqian Zhang
  • Tian Lan
  • Xiaodong He
  • Liu Cao
  • Jia Zhou
  • Jianguo Geng
  • Lijing Wang
چکیده

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 infiltration into solid tumors occurs through a P-selectin-dependent mechanism.

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عنوان ژورنال:

دوره 6  شماره 

صفحات  -

تاریخ انتشار 2015