Research Papers:

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 and Lijing Wang _

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Oncotarget. 2015; 6:6584-6596. https://doi.org/10.18632/oncotarget.3164

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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

Correspondence to:

Lijing Wang, e-mail: [email protected]

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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