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目的:探讨Vav3调节Lewis肺癌细胞增殖及凋亡的作用及机制。方法:小分子干扰RNA(small interfering RNA,siRNA)下调Lewis肺癌细胞中Vav3蛋白的表达;蛋白质印迹法检测转染siRNA-Vav3后Vav3及JNK蛋白表达的变化;MTT方法检测细胞存活率,流式细胞仪检测细胞凋亡。结果:转染siRNA后,干扰组Vav3表达为0.154±0.024,较Lewis肺癌细胞组的0.417±0.073和对照组的0.383±0.049明显下调,F=22.052,P=0.002。下调Vav3表达后,干扰组JNK蛋白表达水平为0.619±0.008,与肺癌细胞组的1.251±0.117和对照组的1.192±0.092相比较明显下调,F=54.770,P<0.001。与肺癌细胞组细胞生存率(100.00±0.00)%和对照组(95.33±3.14)%相比,干扰组(75.87±2.30)%明显下降,P值分别为0.000 2和0.000 3。与肺癌细胞组细胞凋亡率(3.55±0.03)%和对照组(4.18±0.17)%相比,干扰组(12.16±0.02)%明显上升,P值分别为0.000 1和0.000 1。结论:下调Vav3表达,抑制Lewis肺癌细胞的增殖,并且促进肺癌细胞凋亡;Vav3发挥作用可能与JNK信号激活有关。
Objective: To investigate the effect and mechanism of Vav3 on the proliferation and apoptosis of Lewis lung carcinoma cells. Methods: The expression of Vav3 protein in Lewis lung carcinoma cells was down-regulated by small interfering RNA (siRNA). The expression of Vav3 and JNK protein was detected by Western blotting. The cell viability was detected by MTT assay. Cytometry detects apoptosis. Results: After siRNA transfection, the expression of Vav3 in the interference group was 0.154 ± 0.024, significantly lower than that in the Lewis lung carcinoma cell group (0.417 ± 0.073) and the control group (0.383 ± 0.049), F = 22.052, P = 0.002. After down-regulating Vav3 expression, the expression level of JNK protein in interference group was 0.619 ± 0.008, significantly down-regulated compared with 1.251 ± 0.117 in lung cancer cell group and 1.192 ± 0.092 in control group, F = 54.770, P <0.001. Compared with the control group (95.33 ± 3.14)%, the cell survival rate (75.87 ± 2.30)% in the lung cancer cell group decreased significantly (P <0.0002 and 0.0003 respectively) compared with the lung cancer cell group (100.00 ± 0.00)%. Compared with the control group (4.18 ± 0.17)%, the apoptosis rate in the interference group (12.16 ± 0.02)% was significantly higher than that in the lung cancer cell group (3.55 ± 0.03)%, the P values were 0.000 1 and 0.000 1, respectively. Conclusion: The down-regulation of Vav3 expression can inhibit the proliferation of Lewis lung cancer cells and promote the apoptosis of lung cancer cells. Vav3 may be involved in the activation of JNK signaling.