论文部分内容阅读
目的 以胶原蛋白 (CN)作为底物 ,探讨内生肿瘤神经节苷脂 (GS)对神经母细胞LA N5细胞株粘附功能的影响。方法 用葡萄糖苷神经酰氨合成酶抑制剂 (D PDMP)抑制LA N5细胞株GS合成 ,观察该细胞对包被CN粘附作用的变化。结果 暴露于D PDMP 6d后 ,细胞GS几乎完全清除 ,但细胞的活力、增殖率及凋亡率较对照组无明显变化 ;暴露于D -PDMP的细胞 ,其粘附能力仅为对照组的 3 5 % :OD570 分别为 0 .0 7± 0 .0 1和 0 .2 1± 0 .0 3 (P <0 .0 1)。用培养对照组LA N5细胞收集的条件培养液 (其中有细胞脱落的GS)和纯化的肿瘤GSGD2预处理已暴露于D PDMP的LA N5细胞 ,可恢复该细胞的粘附表型 ,较对照组差异无显着性 (P >0 .0 5 )。结论 内生肿瘤GS调节肿瘤细胞对CN的粘附作用 ,提示GS在肿瘤细胞的迁移 ,侵入和转移中可能起重要作用。
Objective To investigate the effect of endogenous tumor gangliosides (GS) on the adhesion of neuroblastoma cell line LA N5 to collagenase (CN) as a substrate. Methods Glucoside ceramide synthase inhibitor (D PDMP) was used to inhibit the GS synthesis of LA N5 cell line and the adhesion of the cell to CN was observed. Results After exposed to D PDMP for 6 days, the cell GS was almost completely eliminated, but the viability, proliferation rate and apoptosis rate of the cells did not change significantly compared with the control group. The adhesion capacity of the cells exposed to D-PDMP was only 3 5%: OD570 were 0.07 ± 0 .0 1 and 0 .2 ± 0 .0 3 (P <0.01). The conditioned medium (with shedding of GS) cultured in control group LA N5 cells and the purified tumor GSGD2 pretreated LA N5 cells exposed to D PDMP restored the cell adhesion phenotype compared with the control group There was no significant difference (P> 0.05). Conclusion Endogenous tumor GS regulates the adhesion of tumor cells to CN, suggesting that GS may play an important role in the migration, invasion and metastasis of tumor cells.