Takemoto Ai, Miyata Kenichi, Fujita Naoya
Division of Experimental Chemotherapy, The Cancer Chemotherapy Center, Japanese Foundation for Cancer Research, 3-8-31, Ariake, Koto-ku, Tokyo, 135-8550, Japan.
Cancer Metastasis Rev. 2017 Jun;36(2):225-234. doi: 10.1007/s10555-017-9672-2.
Tumor cell-induced platelet aggregation facilitates hematogenous metastasis by promoting tumor embolization, preventing immunological assaults and shear stress, and the platelet-releasing growth factors support tumor growth and invasion. Podoplanin, also known as Aggrus, is a type I transmembrane mucin-like glycoprotein and is expressed on wide range of tumor cells. Podoplanin has a role in platelet aggregation and metastasis formation through the binding to its platelet receptor, C-type lectin-like receptor 2 (CLEC-2). The podoplanin research was originally started from the cloning of highly metastatic NL-17 subclone from mouse colon 26 cancer cell line and from the establishment of 8F11 monoclonal antibody (mAb) that could neutralize NL-17-induced platelet aggregation and hematogenous metastasis. Later on, podoplanin was identified as the antigen of 8F11 mAb, and its ectopic expression brought to cells the platelet-aggregating abilities and hematogenous metastasis phenotypes. From the 8F11 mAb recognition epitopes, podoplanin is found to contain tandemly repeated, highly conserved motifs, designated platelet aggregation-stimulating (PLAG) domains. Series of analyses using the cells expressing the mutants and the established neutralizing anti-podoplanin mAbs uncovered that both PLAG3 and PLAG4 domains are associated with the CLEC-2 binding. The neutralizing mAbs targeting PLAG3 or PLAG4 could suppress podoplanin-induced platelet aggregation and hematogenous metastasis through inhibiting the podoplanin-CLEC-2 binding. Therefore, these domains are certainly functional in podoplanin-mediated metastasis through its platelet-aggregating activity. This review summarizes the platelet functions in metastasis formation, the role of platelet aggregation-inducing factor podoplanin in pathological and physiological situations, and the possibility to develop podoplanin-targeting drugs in the future.
肿瘤细胞诱导的血小板聚集通过促进肿瘤栓塞、防止免疫攻击和剪切应力来促进血行转移,并且血小板释放的生长因子支持肿瘤生长和侵袭。血小板结合蛋白(Podoplanin),也称为Aggrus,是一种I型跨膜粘蛋白样糖蛋白,在多种肿瘤细胞上表达。血小板结合蛋白通过与其血小板受体C型凝集素样受体2(CLEC-2)结合,在血小板聚集和转移形成中发挥作用。血小板结合蛋白的研究最初始于从小鼠结肠26癌细胞系中克隆高转移性NL-17亚克隆,以及建立能够中和NL-17诱导的血小板聚集和血行转移的8F11单克隆抗体(mAb)。后来,血小板结合蛋白被鉴定为8F11 mAb的抗原,其异位表达赋予细胞血小板聚集能力和血行转移表型。从8F11 mAb识别表位发现,血小板结合蛋白含有串联重复的、高度保守的基序,称为血小板聚集刺激(PLAG)结构域。使用表达突变体的细胞和已建立的中和抗血小板结合蛋白mAb进行的一系列分析发现,PLAG3和PLAG4结构域均与CLEC-2结合有关。靶向PLAG3或PLAG4的中和mAb可通过抑制血小板结合蛋白-CLEC-2结合来抑制血小板结合蛋白诱导的血小板聚集和血行转移。因此,这些结构域在血小板结合蛋白通过其血小板聚集活性介导的转移中肯定具有功能。本综述总结了血小板在转移形成中的功能、血小板聚集诱导因子血小板结合蛋白在病理和生理情况下的作用,以及未来开发靶向血小板结合蛋白药物的可能性。