P-selectin-mediated platelet adhesion promotes tumor growth

// Cuiling Qi 1, * , Bo Wei 2, * , Weijie Zhou 3, * , Yang Yang 1 , Bin Li 1 , Simei Guo 1 , Jialin Li 1 , Jie Ye 1 , Jiangchao Li 1 , Qianqian Zhang 1 , Tian Lan 1 , Xiaodong He 1 , Liu Cao 4 , Jia Zhou 5 , Jianguo Geng 3 , Lijing Wang 1 1 Vascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, Guangdong 510006, China 2 Department of Gastrointestinal Surgery, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510630, China 3 Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, Michigan 48109, USA 4 Key Laboratory of Medical Cell Biology, China Medical University, Shen Yang City, Liao Ning Province 110001, China 5 Chemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, Texas 77555, USA * These authors have contributed equally to this work Correspondence to: Lijing Wang, e-mail: wanglijing62@163.com Keywords: P-selectin, platelets, tumor growth, αIIbβ3, talin1 Received: September 15, 2014      Accepted: January 19, 2015      Published: February 09, 2015 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 αIIbβ3 and recruits platelets into tumors. Platelet infiltration into solid tumors occurs through a P-selectin-dependent mechanism.