P-selectin-mediated platelet adhesion promotes tumor growth

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

Research output: Contribution to journalArticlepeer-review

37 Scopus citations


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 languageEnglish (US)
Pages (from-to)6584-6596
Number of pages13
Issue number9
StatePublished - 2015


  • P-selectin
  • Platelets
  • Talin1
  • Tumor growth
  • aIIbβ3

ASJC Scopus subject areas

  • Oncology


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