P-selectin-mediated platelet adhesion promotes tumor growth
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Cuiling Qi1,*, Bo Wei2,*, Weijie Zhou3,*, Yang Yang1, Bin Li1, Simei Guo1, Jialin Li1, Jie Ye1, Jiangchao Li1, Qianqian Zhang1, Tian Lan1, Xiaodong He1, Liu Cao4, Jia Zhou5, Jianguo Geng3, Lijing Wang1
1Vascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, Guangdong 510006, China
2Department of Gastrointestinal Surgery, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510630, China
3Department of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, Michigan 48109, USA
4Key Laboratory of Medical Cell Biology, China Medical University, Shen Yang City, Liao Ning Province 110001, China
5Chemical Biology Program, Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, Texas 77555, USA
*These authors have contributed equally to this work
Lijing Wang, e-mail: firstname.lastname@example.org
Keywords: P-selectin, platelets, tumor growth, αIIbβ3, talin1
Received: September 15, 2014 Accepted: January 19, 2015 Published: February 09, 2015
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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