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目的研究细胞信号转导抑制因子1(SOCS1)基因表达抑制对人舌鳞癌细胞侵袭、迁移及凋亡的影响。方法人舌鳞癌细胞系CAL27中SOCS1沉默效果采用实时定量PCR和Western blotting方法验证;应用Transwell侵袭小室模型观察舌鳞癌细胞的侵袭力;划痕试验检测细胞迁移能力;流式细胞术检测细胞凋亡率,Western blotting检测Bax、Bcl-2、Caspase-3蛋白表达水平。结果 SOCS1干扰片段显著下调CAL27细胞SOCS1基因的蛋白和m RNA表达水平(P<0.05)。沉默SOCS1表达后,干扰组和对照组细胞体外穿膜细胞数分别为(42±9)个和(91±17)个,迁移细胞数分别为(93±14)个和(184±3)个,干扰组均明显弱于对照组(P<0.05);SOCS1表达抑制后CAL27细胞凋亡率(11.5±2.1)%明显大于对照组(1.3±0.4)%,且凋亡相关蛋白Bax、Caspase-3表达水平显著升高,Bcl-2蛋白表达水平下降,与对照组比较差异均有统计学意义(P<0.05)。结论人舌鳞癌细胞株CAL27的SOCS1基因表达抑制后,体外侵袭、迁移能力下降,且促进舌鳞癌细胞凋亡。
Objective To investigate the effect of suppression of cell signal transduction inhibitor 1 (SOCS1) gene expression on invasion, migration and apoptosis of human tongue squamous cell carcinoma. Methods The silencing effects of SOCS1 in human tongue squamous cell carcinoma cell line CAL27 were confirmed by real-time PCR and Western blotting. Transwell invasive chamber model was used to observe the invasiveness of tongue squamous carcinoma cells. Scratch test was used to detect the migration ability of cells. Flow cytometry The apoptosis rate and Western blotting were used to detect the protein expression of Bax, Bcl-2 and Caspase-3. Results SOCS1 knockdown significantly down-regulated the protein and mRNA expression of SOCS1 in CAL27 cells (P <0.05). After silencing SOCS1 expression, the number of transmembrane cells in vitro and in vivo were (42 ± 9) and (91 ± 17), respectively, and the numbers of migrating cells were (93 ± 14) and (184 ± 3) (P <0.05). The apoptosis rate of CAL27 cells after SOCS1 expression was (11.5 ± 2.1)% was significantly higher than that of control group (1.3 ± 0.4)%, and the apoptosis related proteins Bax and Caspase- 3 expression was significantly increased, Bcl-2 protein expression levels decreased compared with the control group were statistically significant (P <0.05). Conclusion Inhibition of SOCS1 gene expression in human tongue squamous cell carcinoma cell line CAL27 decreases the ability of invasion and migration in vitro and promotes the apoptosis of tongue squamous cell carcinoma.