Qi Cuiling, Wei Bo, Zhou Weijie, Yang Yang, Li Bin, Guo Simei, Li Jialin, Ye Jie, Li Jiangchao, Zhang Qianqian, Lan Tian, He Xiaodong, Cao Liu, Zhou Jia, Geng Jianguo, Wang Lijing
Vascular Biology Research Institute, Guangdong Pharmaceutical University, Guangzhou, Guangdong 510006, China.
Department of Gastrointestinal Surgery, The Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510630, China.
Oncotarget. 2015 Mar 30;6(9):6584-96. doi: 10.18632/oncotarget.3164.
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.
血小板促进癌症发生。我们发现血小板在人类肿瘤中聚集。P-选择素缺乏和可溶性P-选择素可消除肿瘤内血小板的沉积，减少血管内皮生长因子的分泌和血管生成，从而抑制肿瘤生长。P-选择素细胞质尾巴与踝蛋白1结合会触发踝蛋白1的N端头部与β3细胞质尾巴相互作用。这会激活αIIbβ3并将血小板募集到肿瘤中。血小板浸润实体瘤是通过一种依赖P-选择素的机制发生的。
