P-selectin-mediated platelet adhesion promotes tumor growth

被引:71
|
作者
Qi, Cuiling [1 ]
Wei, Bo [2 ]
Zhou, Weijie [3 ]
Yang, Yang [1 ]
Li, Bin [1 ]
Guo, Simei [1 ]
Li, Jalin [1 ]
Ye, Jie [1 ]
Li, Jiangchao [1 ]
Zhang, Qianqian [1 ]
Lan, Tian [1 ]
He, Xiaodong [1 ]
Cao, Liu [4 ]
Zhou, Jia [5 ]
Geng, Jianguo [3 ]
Wang, Lijing [1 ]
机构
[1] Guangdong Pharmaceut Univ, Vasc Biol Res Inst, Guangzhou 510006, Guangdong, Peoples R China
[2] Sun Yat Sen Univ, Dept Gastrointestinal Surg, Affiliated Hosp 3, Guangzhou 510630, Guangdong, Peoples R China
[3] Univ Michigan, Sch Dent, Dept Biol & Mat Sci, Ann Arbor, MI 48109 USA
[4] China Med Univ, Key Lab Med Cell Biol, Shen Yang City 110001, Liao Ning Provi, Peoples R China
[5] Univ Texas Med Branch, Chem Biol Program, Dept Pharmacol & Toxicol, Galveston, TX 77555 USA
基金
美国国家科学基金会;
关键词
P-selectin; platelets; tumor growth; alpha IIb beta 3; talin1; IN-VIVO; METASTASIS FORMATION; CANCER GROWTH; ANGIOGENESIS; ACTIVATION; LEUKOCYTES; CARCINOMA; MODEL; INHIBITION; GPIIB/IIIA;
D O I
10.18632/oncotarget.3164
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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 beta 3 cytoplasmic tail. This activates alpha IIb beta 3 and recruits platelets into tumors. Platelet infiltration into solid tumors occurs through a P-selectin-dependent mechanism.
引用
收藏
页码:6584 / 6596
页数:13
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