CXCL8/CXCR1驱动FOXS1蛋白促进食管癌ECA109细胞增殖、侵袭及迁移  

CXCL8/CXCR1 promotes the proliferation, invasion, and migration of esophageal cancer cell ECA109 by regulating the FOXS1 protein

作　　者：李丽丽 刘婷隽 LI Li-li;LIU Ting-jun(International College,Yellow River University of Science and Technology,Zhengzhou 450000,China;Animal Erperiment Center,Xuzhou Medical University,Xuzhou 221000,China)

机构地区：[1]黄河科技学院国际学院,郑州450000 [2]徐州医科大学动物实验中心,徐州221000

出　　处：《现代免疫学》2023年第2期137-143,共7页Current Immunology

基　　金：河南省2018年科技发展计划项目(182102310100)。

摘　　要：为了探讨CXC趋化因子配体8(CXC motif chemokine ligand 8,CXCL8)/CXC趋化因子受体1(CXC chemokine receptor 1,CXCR1)对体外人食管癌细胞ECA109增殖、凋亡及侵袭迁移的影响,并观察其与叉头框家族S1(forkhead box S1,FOXS1)蛋白的关系,将人食管癌细胞ECA109转染后分为对照组、CXCL8组、CXCL8+Con-siRNA组和CXCL8+CXCR1-siRNA组。CXCL8终浓度为10μg/mL。采用MTT试验检测细胞增殖情况,克隆试验检测克隆形成情况,流式细胞仪进行细胞凋亡测试,侵袭与迁移能力由Transwell试验和划痕试验测定,Western blotting检测细胞中CXCR1、FOXS1蛋白表达水平。结果显示,与对照组比较,CXCL8能够显著促进ECA109细胞增殖、克隆、侵袭和迁移(P<0.05),而干扰CXCR1后这些作用被阻断(P<0.05)。CXCL8组、CXCL8+Con-siRNA组细胞凋亡率与对照组比较,差异无统计学意义(P>0.05),CXCL8+CXCR1-siRNA组细胞凋亡率显著下降(P<0.05)。与对照组比较,CXCL8能够上调食管癌细胞CXCR1和FOXS1蛋白表达(P<0.05),而干扰CXCR1后CXCR1和FOXS1蛋白表达均出现显著下降(P<0.05)。该研究提示,CXCL8/CXCR1可促进食管癌细胞增殖、侵袭和迁移,其作用可能与驱动FOXS1蛋白有关。This study aims to study the effects of CXC motif chemokine ligand 8(CXCL8)/CXC chemokine receptor 1(CXCR1) on the proliferation, apoptosis, invasion, and migration of human esophageal cancer cell ECA109 in vitro, and to explore the relationship between CXCL8/CXCR1 and forkhead box S1(FOXS1) protein. The human esophageal cancer cells ECA109 were divided into control group, CXCL8 group, CXCL8+Con-siRNA group, and CXCL8+CXCR1-siRNA group after cell transfection. The final concentration of CXCL8 in each group was 10 μg/mL. MTT assay was used to detect cell proliferation;cloning assay was used to detect clone formation and flow cytometry was used to measure cell apoptosis. The invasion and migration of the cells were evaluated by Transwell assay and scratch assay, respectively. In addition, the protein levels of CXCR1 and FOXS1 were detected by Western blotting. The results showed that, compared to cells in the control group, CXCL8 significantly promoted the proliferation, cell cloning, invasion, and migration of ECA109 cells(P<0.05). However, this effect was blocked by CXCR1 interference(P<0.05). There were no significant differences in cell apoptosis in the CXCL8 group when compared to either the CXCL8+Con-siRNA group or the control group(P>0.05), whereas the cell apoptosis decreased significantly in CXCL8+CXCR1-siRNA group(P<0.05). Esophageal cancer cells in the CXCL8 group showed upregulated expression of CXCR1 and FOXS1 proteins compared to those in the control group(P<0.05). However, both CXCR1 and FOXS1 protein expressions were significantly decreased after interfering with CXCR1(P<0.05). Altogether, the results suggest that CXCL8/CXCR1 promotes the proliferation, invasion, and migration of esophageal cancer cells in vitro, possibly by regulating FOXS1 protein expression.

关 键 词：CXC趋化因子配体8/CXC趋化因子受体1 叉头框家族S1 食管癌细胞ECA109 增殖 凋亡 侵袭 迁移 

分 类 号：R735.1[医药卫生—肿瘤]