XIAP基因对TNF-α诱导的鼻咽癌细胞凋亡及VEGF和COX-2表达的机制研究  

Study on the mechanism of XIAP gene on TNF-α-induced apoptosis and expression of VEGF and COX-2 in nasopharyngeal carcinoma cells

作　　者：梁猛 LIANG Meng(Department of Oncology,Shiyan Taihe Hospital Affiliated to Hubei Medical College,Shiyan Hubei 442000,China)

机构地区：[1]湖北医药学院附属医院十堰市太和医院肿瘤科,湖北十堰442000

出　　处：《蚌埠医学院学报》2022年第3期284-288,共5页Journal of Bengbu Medical College

摘　　要：目的:探讨X连锁凋亡抑制蛋白(XIAP)基因对肿瘤坏死因子α(TNF-α)诱导的鼻咽癌细胞凋亡及血管内皮生长因子(VEGF)和环氧化酶-2(COX-2)表达的影响。方法:将人鼻咽癌5-8F细胞分为空白组、TNF-α组(10 ng/mL的外源性TNF-α处理5-8F细胞12 h)、si-XIAP组(si-XIAP转染5-8F细胞48 h)和TNF-α+si-XIAP(si-XIAP转染5-8F细胞48 h后,使用10 ng/mL的外源性TNF-α处理细胞12 h)。Western blotting检测XIAP、VEGF、COX-2、Cleaved caspase3、Bax、NF-κB p65和Ikkβ蛋白表达;MTT法及流式细胞术分别检测细胞活力和凋亡率。结果:转染si-XIAP的5-8F细胞XIAP表达明显低于空白组(P<0.01)。TNF-α组和si-XIAP组细胞活力低于空白组(P<0.05),细胞凋亡率及Cleaved caspase3和Bax表达均高于空白组(P<0.05)。TNF-α组VEGF、COX-2、NF-κB p65和Ikkβ表达均高于空白组(P<0.05)。si-XIAP组VEGF、COX-2、NF-κB p65和Ikkβ表达均低于空白组(P<0.05)。TNF-α+si-XIAP组细胞活力低于TNF-α组和si-XIAP组(P<0.05);VEGF、COX-2、NF-κB p65和Ikkβ表达均低于TNF-α组、高于si-XIAP组(P<0.05);细胞凋亡率及Cleaved caspase3和Bax表达均高于TNF-α组和si-XIAP组(P<0.05)。结论:下调XIAP基因表达增强TNF-α诱导的鼻咽癌5-8F细胞凋亡及降低VEGF和COX-2表达,机制与抑制NF-κB信号通路有关。Objective:To investigate the effect of X-linked inhibitor of apoptosis protein(XIAP)gene on the tumor necrosis factor-α(TNF-α)-induced apoptosis,and expression of vascular endothelial growth factor(VEGF)and cyclooxygenase-2(COX-2)in nasopharyngeal carcinoma cells.Methods:Human nasopharyngeal carcinoma 5-8F cells were divided into blank group,TNF-αgroup(cells treated with 10 ng/mL exogenous TNF-αfor 12 h),si-XIAP group(cells transfected with si-XIAP for 48 h)and TNF-α+si-XIAP(cells transfected with si-XIAP for 48 h,then treated with 10 ng/mL exogenous TNF-αfor 12 h).Western blotting was used to detect the protein expression of XIAP,VEGF,COX-2,Cleaved caspase3,Bax,NF-κB p65 and Ikkβ.MTT assay and flow cytometry were used to detect cell viability and apoptosis rate.Results:The expression of XIAP in 5-8F cells transfected with si-XIAP was significantly lower than that in blank group(P<0.01).The cell viability in TNF-αgroup and si-XIAP group was lower than that in blank group(P<0.05),and the apoptosis rate and the expression of Cleaved caspase3 and Bax were higher than those in blank group(P<0.05).The expressions of VEGF,COX-2,NF-κB p65 and Ikkβin TNF-αgroup were higher than those in blank group(P<0.05).The expressions of VEGF,COX-2,NF-κB p65 and Ikkβin si-XIAP group were lower than those in blank group(P<0.05).The cell viability in TNF-α+si-XIAP group was lower than that in TNF-αgroup and si-XIAP group(P<0.05);the expressions of VEGF,COX-2,NF-κB p65 and Ikkβwere lower than those in TNF-αgroup and higher than those in si-XIAP group(P<0.05);the apoptosis rate and the expression of Cleaved caspase3 and Bax were higher than those in TNF-αgroup and si-XIAP group(P<0.05).Conclusions:Down-regulating the expression of XIAP gene enhances TNF-α-induced apoptosis and reduces the expression of VEGF and COX-2 in nasopharyngeal carcinoma 5-8F cells,which is related to the inhibition of NF-κB signaling pathway.

关 键 词：鼻咽肿瘤 X连锁凋亡抑制蛋白 肿瘤坏死因子α 细胞凋亡 

分 类 号：R739.6[医药卫生—肿瘤]