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目的:研究成纤维激活蛋白(Fibroblast Activation Protein,FAP)在促进卵巢癌细胞发生侵袭、迁移、增殖过程中与整合素α3β1、尿激酶型纤溶酶原激活剂受体(uPAR)的关系。方法:1).免疫共沉淀共同检测整合素α3β1、uPAR在HO-8910PM上是否为二聚体。2).transwell侵袭实验、迁移实验检测抑制整合素α3β1、uPAR后,卵巢癌细胞系HO-8910PM的侵袭迁移能力;3).抑制整合素α3β1、uPAR后,再给予FAPα对HO-8910PM侵袭、迁移和增殖的影响。结果:1).整合素α3β1、uPAR在HO-8910PM细胞外同一个位置表达;2).抑制整合素α3β1能够明显抑制HO-8910PM的侵袭、迁移、增殖能力,并且可以抑制FAP对肿瘤的作用。3).PAI-1抑制uPAR后,HO-8910PM的侵袭、迁移、增殖无明显变化,同时对FAP也无明显作用。结论:整合素α3β1和uPAR在HO-8910PM是一个复合体,FAPα在细胞外是通过整合素α3β1传递信号进入细胞内而不是通过uPAR,整合素α3β1是通过uPAR与肿瘤细胞相连接。
OBJECTIVE: To investigate the relationship between fibroblast activation protein (FAP) and integrin α3β1 and urokinase-type plasminogen activator receptor (uPAR) in the process of invasion, migration and proliferation of ovarian cancer cells. Methods: 1) co-immunoprecipitation co-detection of integrin α3β1, uPAR in HO-8910PM is a dimer. 2) .transwell invasion assay, migration assay to detect the invasion and migration of ovarian cancer cell line HO-8910PM after inhibition of integrinα3β1, uPAR; 3) Inhibition of integrinα3β1, uPAR, Effects of migration and proliferation. Results: 1) Integrin α3β1 and uPAR were expressed in the same location outside HO-8910PM cells; 2) Inhibition of integrin α3β1 significantly inhibited the invasion, migration and proliferation of HO-8910PM and inhibited the effect of FAP on tumor . 3) .PAI-1 inhibited uPAR, HO-8910PM invasion, migration, proliferation no significant change, while no significant effect on FAP. CONCLUSIONS: Integrin α3β1 and uPAR are a complex at HO-8910PM. FAPα translocates to the cell via integrin α3β1 rather than uPAR, and integrin α3β1 is linked to tumor cells via uPAR.