目的探讨PSMA7表达量的变化对A549细胞表面黏附分子ICAM-1,VCAM-1和CD44表达的影响。方法采用流式细胞仪分别检测高表达PSMA7的A549细胞[pcDNA3.1(-)/PSMA7组1和低表达PSMA7的A549细胞(shPSMA7组)表面黏附分子ICAM-1,VCAM-1和CD44的表达情况。结果与高表达阴性对照组[pcDNA3.1(-)组1相比,pcDNA3.1(-)/PSMA7组的ICAM-10=86.325,P=-0.000)和VCAM-l(t=16.337,P=0.000)的表达量均显著降低,CD44表达量则无明显变化(t=-0.545,P=0.615),而与低表达阴性对照组(shNC组)相比,shPSMA7组ICAM-1(t=-119.827,P=-0.000)和VCAM-1(t=26.68,P=0.000)表达量均显著增高,CD44表达量则无明显变化(t=-848,P=-0.4441。与pcDNA3.1f-1组相比,pcDNA3.1(-)/PSMA7组穿膜侵袭细胞的数量明显减少(t=3.553,P=0.024),而shPSMA7组明显高于shNC组(t=-3.207,P=0.0331。结论高表达或干扰PSMA7可影响A549细胞表面黏附分子ICAM-1,VCAM-1的表达,提示PSMA7可能因此参与肺腺癌细胞的侵袭和转移。
To observe the effect of PSMA7 changes on adhesion molecule expression on A549 cell, flow cytometry was used to detect the expression of ICAM-1, VCAM-1 and CD44 in pcDNA3.1(-)/PSMA7 A549 cell line and shPSMA7 A549 cell line. Compared with pcDNA3.1(-) group, the expression of ICAM-1 (t=86.325, P= 0.000) and VCAM-1 (t=16.337, P=0.000) in pcDNA3.1(-)/PSMA7 group was significantly decreased, but CD44 expression (t=-0.545, P=0.615) did not change; compared with shNC group, the expression of ICAM-1 (t=-119.827, P=0.000) and VCAM-1 (t=-26.68, P=0.000) in shPSMA7 group was significantly increased, but CD44 expression (t=-848, P=0.444) did not change; compared with pcDNA3.1(-) group, the number of migrated A549 cells in pcDNA3.1(-)/PSMA7 group was significantly decreased (t=3.553,P=0.024); and compared with shNC group, migrated A549 cells of shPSMA7 group significantly increased (t=-3.207,P=0.033). In conclusion, over- and low- expression of PSMA7 maybe affect the expression of adhesion molecule ICAM-1 and VCAM-1 in A549 cell line.