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目的 探讨血小板在肝癌转移中的作用、地位及可能机制。方法 采用体外细胞粘附及粘附抑制实验 ,分别比较血小板对高、低转移潜能人肝癌细胞株MHCC97、SMMC772 1与细胞外基质 (ECM)蛋白粘附的影响 ,研究血小板粘附分子在其中的作用。结果 血小板活化与否不改变SMMC772 1、MHCC97细胞与ECM的粘附 ;血小板不影响SMMC772 1细胞与ECM的粘附 ,但可明显增强MHCC97细胞与ECM的粘附 (P <0 0 1) ;血小板粘附分子P selectin和GPⅡb Ⅲa在活化血小板对SMMC772 1细胞与ECM的粘附影响中可能无明显作用 ,但干扰其作用可明显抑制活化血小板对MHCC97细胞与ECM粘附的增强作用 (P <0 0 5 ,P <0 0 1)。而SMMC772 1细胞与ECM或血小板包被的ECM的粘附能力均明显低于MHCC97细胞 (P <0 0 5 ,P <0 0 1) ;P selectin单抗、GPⅢa单抗作用于活化血小板包被的ECM后 ,其与SMMC772 1细胞的粘附仍低于其与MHCC97细胞的粘附 (P <0 0 5 ) ,而GPⅡb单抗作用后 ,二者间粘附无明显差异 (P >0 0 5 )。结论 血小板可明显增强MHCC97细胞与ECM的粘附 ;活化血小板包被的ECM与MHCC97细胞的粘附增强作用可能由血小板P selectin、GPⅡb Ⅲa所介导。
Objective To investigate the role, status and possible mechanism of platelets in the metastasis of liver cancer. Methods In vitro cell adhesion and adhesion inhibition experiments were performed to compare the effects of platelets on the adhesion of MHCC97, SMMC772 1 cells to extracellular matrix (ECM) in high and low metastatic potential human hepatoma cell lines, respectively. The effects of platelet adhesion molecules on effect. Results Platelet activation did not change the adhesion of SMCC772 1 and MHCC97 cells to ECM. Platelets did not affect the adhesion of SMMC772 1 cells to ECM, but significantly enhanced the adhesion of MHCC97 cells to ECM (P <0.01) The adhesion molecules P selectin and GPⅡb Ⅲa may have no significant effect on the adhesion of SMMC772 1 cells to ECM by activated platelets, but their effects may inhibit the enhancement of the adhesion of activated platelets to ECM (P <0) 0 5, P <0 0 1). However, the adhesion ability of SMMC772 1 cells to ECM or platelet-coated ECM was significantly lower than that of MHCC97 cells (P <0.05, P <0.01). P selectin monoclonal antibody and GPIIIa monoclonal antibody were applied to activated platelet coating ECM, the adhesion to SMMC772 1 cells was still lower than that to MHCC97 cells (P <0 05), while there was no significant difference between them (P 0 0 0) 5). Conclusion Platelets can significantly enhance the adhesion of MHCC97 cells to ECM. The enhanced adhesion of activated platelet-coated ECM to MHCC97 cells may be mediated by P selectin and GPⅡb Ⅲ a.