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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]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]相比,pcDNA3.1(-)/PSMA7组的ICAM-1(t=86.325,P=0.000)和VCAM-1(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=0.444)。与pcDNA3.1(-)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=0.033)。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。
Objective To investigate the effect of PSMA7 expression on the expression of ICAM-1, VCAM-1 and CD44 on A549 cells. Methods Flow cytometry was used to detect the expression of ICAM-1, VCAM-1 and CD44 on the surface of A549 cells (pcDNA3.1 (-) / PSMA7 group) and PSMA7-low A549 cells (shPSMA7 group) Happening. Results ICAM-1 (t = 86.325, P = 0.000) and VCAM-1 in pcDNA3.1 (-) / PSMA7 group were higher than those in pcDNA3.1 (- (T = -0.545, P = 0.615). Compared with the shNCMA negative control group (shNC group), the expression of ICAM-1 (t = -119.827, P = 0.000) and VCAM-1 (t = -26.68, P = 0.000), but there was no significant change in the expression of CD44 (t = -848, P = 0.444). The number of invasive cells in pcDNA3.1 (-) / PSMA7 group was significantly lower than that in pcDNA3.1 (-) group (t = 3.553, P = 0.024) 3.207, P = 0.033). Conclusion High expression or interference of PSMA7 can affect the expression of ICAM-1 and VCAM-1 on the surface of A549 cells, suggesting that PSMA7 might participate in the invasion and metastasis of lung adenocarcinoma cells.