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目的探讨蛋白激酶C(PKC)抑制剂星型胞菌素(staurosporine,STS)对肺腺癌A549细胞体外黏附能力的影响及作用机制。方法采用STS处理A549细胞,检测细胞黏附能力的变化;western blot检测黏附分子E-cadherin(E-Cad)、in-tegrinβ1、Laminin Receptor(LnR)蛋白含量以及细胞浆、细胞膜PKC-α蛋白含量变化。结果黏附实验显示,STS抑制A549细胞对Matrigel的黏附,抑制率随STS浓度增大而增加,10 nmol.L-1和100 nmol.L-1STS的抑制率达到50%和74%(均P<0.01)。Western blot结果显示A549细胞经100 nmol.L-1STS作用24 h,E-cad、integrinβ1和LnR蛋白含量分别为对照组的2.91倍、0.44倍和0.57倍(均P<0.01);细胞膜PKC-α蛋白含量减少,为对照组的22.73%(P<0.01),胞浆PKC-α蛋白含量与对照组比较,差异无显著性(P>0.05)。结论 STS通过诱导肿瘤细胞E-Cad表达和抑制integrinβ1、LnR表达来抑制A549细胞黏附能力;STS对上述细胞黏附的影响可能与PKC-α的活性抑制相关。
Objective To investigate the effect of protein kinase C (PKC) inhibitor staurosporine (STS) on the adhering capacity of lung adenocarcinoma A549 cells in vitro and its mechanism of action. Methods A549 cells were treated with STS to detect the changes of cell adhesion ability. Western blot was used to detect the contents of E-cadherin (E-Cad), in-tegrinβ1 and Laminin Receptor (LnR) proteins, and the changes of cytoplasm and plasma membrane PKC-α protein levels. . Results Adhesion experiments showed that STS inhibited the adhesion of A549 cells to Matrigel, and the inhibition rate increased with the increase of STS concentration. The inhibition rates of 10 nmol.L-1 and 100 nmol.L-1STS reached 50% and 74% (P< 0.01). Western blot results showed that the A549 cells were treated with 100 nmol.L-1STS for 24 h and the E-cad, integrin β1 and LnR protein levels were 2.91, 0.44, and 0.57 times of the control group, respectively (all P<0.01); the plasma membrane PKC-α The decrease of protein content was 22.73% (P<0.01) in the control group. Compared with the control group, there was no significant difference in cytoplasmic PKC-α protein content (P>0.05). Conclusion STS inhibits the adhesion of A549 cells by inducing the expression of E-Cad and inhibiting the expression of integrinβ1 and LnR. The effect of STS on cell adhesion may be related to the inhibition of PKC-α activity.