干扰素诱导蛋白10对舌鳞癌细胞增殖、凋亡的影响

目的: 探讨干扰素诱导蛋白10（IP-10）对舌鳞癌细胞CAL-27增殖、凋亡的影响以及与CXCR3A、CXCR3B基因表达的关系。方法: 将CAL-27 细胞分为 3 个实验组和 1 个对照组,3 个实验组分别采用10、20、40 ng/mL 的IP-10刺激,对照组不予刺激。刺激12、24、48、72 h时,利用CCK-8法检测 4 组细胞的增殖活性;24 h 时,利用流式细胞仪检测细胞凋亡。采用Q-PCR检测10 ng/mL IP-10作用下,CAL-27细胞在12、24、48、72 h时CXCR3A、CXCR3B mRNA的表达情况。采用SPSS16.0软件包对数据进行单因素方差分析。结果: 12 h和24 h 时,3种浓度的IP-10 均能促进 CAL-27 细胞增殖（P<0.05）;在 48 h 时,只有40 ng/mL的 IP-10 能够促进 CAL-27 细胞增殖（P<0.01）; 而在72 h时,3种浓度的 IP-10对 CAL-27 细胞的增殖均无促进作用（P>0.05）。24 h后,3个实验组与对照组相比,CAL-27细胞的增殖率降低。24 h 时,3种实验组细胞凋亡率分别为（3.377±0.575）%、（6.867±2.848）%和（5.317±2.794）%,与对照组相比具有显著差异（P<0.05）,但各实验组间无显著差异（P>0.05)。12、24、48、72 h时,CXCR3A mRNA的表达量分别为0.0130±0.0007、0.0274±0.0005 、0.0204±0.0011和0.0174±0.0006,组间差异显著（P<0.05）;CXCR3B mRNA的表达量分别为0.0124±0.0015、0.0209±0.0016、0.0297±0.0013和0.0386±0.0010,组间差异显著（P<0.05）。结论: IP-10既能促进舌鳞癌细胞CAL-27增殖又能够诱导其凋亡,随着作用时间的推移,细胞增殖率降低;CXCR3A mRNA的表达先升高后降低,而CXCR3B mRNA的表达逐渐升高。CXCR3A、CXCR3B可能参与调控IP-10诱导下的舌鳞癌细胞的增殖和凋亡。

Effect of interferon inducible protein-10 on proliferation and apoptosis of tongue squamous cancer cell

PURPOSE: To investigate the influence of interferon inducible protein-10 (IP-10) on proliferation, apoptosis of tongue squamous cancer cell CAL-27 , and the relation with CXCR3A, CXCR3B gene expression. METHODS: CAL-27 cells were divided into 3 experimental group and 1 control group. The experimental groups were treated with 10 ng/mL, 20 ng/mL, and 40 ng/mL IP-10, respectively; while the control group was not stimulated. CCK 8 was used to test cell proliferation after being stimulated for 12, 24, 48, and 72 h; Flow cytometry was used to detect cell apoptosis after being stimulated for 24 h. Q-PCR was used to detect CXCR3A, CXCR3B mRNA expression after being stimulated for 12, 24, 48 and 72 h, respectively. SPSS 16.0 software package was used for statistical analysis. RESULTS: IP-10 with 3 kinds of concentration promoted CAL-27 cell proliferation (P<0.05) at 12, 24 h. At 48h, only 40 ng/mL of IP-10 promoted CAL-27 cell proliferation (P<0.01). At 72 h, IP-10 with 3 kinds of concentration had no effect on CAL-27 cell proliferation (P>0.05). After 24 h, CAL 27 cell proliferation in 3 experimental groups decreased compared with the control group. At 24 h, cell apoptosis rate in 3 experimental groups was 3.377%±0.575%, 6.867%±2.848%, 5.317%±2.794%, respectively. There was significant difference between the control group (P<0.05), but no significant difference between the experimental groups (P>0.05). At 12, 24, 48, 72 h, CXCR3A mRNA expression was 0.0130±0.0007, 0.0274±0.0005, 0.0204±0.0011 and 0.0174±0.0006 respectively; there was significant difference between groups (P<0.05). CXCR3B mRNA expression was 0.0124±0.0015, 0.0209±0.0016, 0.0297±0.0013 and 0.0386±0.0010, respectively; there was significant difference between groups (P<0.05). CONCLUSIONS: IP-10 can not only promote CAL-27 proliferation, but also induce its apoptosis. As time goes on, cell proliferation decreased, CXCR3A mRNA expression increased first and then decreased, while CXCR3B mRNA expression increased gradually. CXCR3A, CXCR3B may participate in regulation of tongue squamous cancer cell proliferation and apoptosis induced by IP-10.