没食子酸抑制人舌鳞癌SCC-9细胞增殖、凋亡及可能机制研究

Gallic acid inhibits the proliferation and apoptosis of oral cancer cell line SCC-9 and its possible mechanism

目的观察没食子酸(GA)对人舌鳞癌细胞SCC-9增殖、凋亡的影响,并探讨其可能机制。方法将SCC-9细胞分为对照组和低、中、高浓度没食子酸组(30、60、90μM GA组)。采用MTT法检测细胞增殖;流式细胞仪检测SCC-9细胞周期及凋亡率;TUNEL法检测细胞凋亡;Western blot检测SCC-9细胞中Cleaved-caspase9、Cleaved-caspase8、Cleaved-caspase3、Cleaved-PARP、p-ERK1/2、p-JNK1/2和p-P38蛋白表达。结果与对照组比较,低、中、高浓度没食子酸组SCC-9细胞增殖率逐渐下降,而sub G1期DNA含量、细胞凋亡率以及阳性凋亡细胞数逐渐增加,呈剂量依赖性;与对照组比较,没食子酸组Cleaved-caspase9、Cleaved-caspase8、Cleaved-caspase3、Cleaved-PARP、p-ERK1/2、p-JNK1/2和p-P38蛋白表达均逐渐增加(P<0.05),呈剂量依赖性。结论没食子酸具有抑制SCC-9细胞增殖、诱导凋亡作用,其机制可能与激活MAPK/ERK信号通路,磷酸化下游Caspase信号因子有关。

Objective To observe the effect of GA on the proliferation and apoptosis of SCC-9 cells and explore its possible mechanism.Methods The SCC-9 cells were divided into control group,and low,medium and high concentration gallic acid groups(30,60,90μM GA).Cell proliferation was detected by MTT assay.The cell cycle and apoptosis rate of SCC-9 were detected by flow cytometry.The apoptosis of SCC-9 cells in each group was detected by TUNEL method.The expressions of Cl-caspase9,Cl-caspase8,Cl-caspase3,Cl-PARP,p-ERK1/2,p-JNK1/2 and p-p38 in SCC-9 cells were detected by Western blotting.Results Compared with the control group,the proliferation rate of SCC-9 cells in low,medium and high concentration gallic acid group decreased gradually,while the DNA content in sub G1 phase,apoptosis rate and the number of positive apoptotic cells increased gradually in a dose-dependent manner.Compared with the control group,the protein expression of Cl-caspase9,Cl-caspase8,Cl-caspase3,Cl-PARP,p-ERK1/2,p-JNK1/2 and p-P38 in the gallic acid group was gradually increased in a dose-dependent manner(P<0.05).Conclusion GA can inhibit the proliferation and induce apoptosis of SCC-9 cells,and its mechanism may be related to activation of MAPK/ERK signaling pathway and phosphorylation of downstream caspase signaling factors.