趋化因子CXCL1对人宫颈癌细胞活性的影响及分子机制  

Effect of Chemokine CXCL1 on Activity of Human Cervical Cancer Cells and Its Molecular Mechanism

作　　者：闫嘉营 YAN Jiaying(th People’s Hospital in Qinghai Province,Xining 810007,China)

机构地区：[1]青海省第四人民医院,青海西宁810007

出　　处：《北华大学学报（自然科学版）》2022年第1期59-63,共5页Journal of Beihua University（Natural Science）

基　　金：青海省科技发展计划项目(2019ZJ760).

摘　　要：目的探讨趋化因子CXCL1对人宫颈癌细胞活性的影响及分子机制.方法将体外培养人宫颈癌细胞株C33A细胞分为对照组(常规培养基)、CXCL1组(25、50、100 ng/mL)、pd98060组(100μmol/L pd98060)、CXCL1+pd98060组(100 ng/mL CXCL1+100μmol/L pd98060).应用MTT法检测细胞增殖能力,应用划痕实验和Transwell侵袭实验检测细胞迁移和侵袭能力;应用Western blot检测磷酸化细胞外信号调节激酶(p-ERK)、细胞外信号调节激酶(ERK)、E26转录因子蛋白1(ETS-1)、基质金属蛋白酶2(MMP-2)表达.结果CXCL1组宫颈癌细胞增殖水平、增殖率、侵袭率明显高于对照组(P<0.01);趋化因子CXCL1呈浓度依赖性地促进宫颈癌细胞的增殖、迁移和侵袭;CXCL1+pd98059组宫颈癌细胞增殖水平、增殖率、侵袭率明显低于CXCL1组(100 ng/mL)(P<0.01);pd98060组宫颈癌细胞增殖水平、增殖率、侵袭率明显低于CXCL1+pd98059组,差异具有统计学意义(P<0.01).随着趋化因子CXCL1作用时间的延长,p-ERK蛋白表达水平明显增加(P<0.01).CXCL1组p-ERK表达水平明显高于对照组,CXCL1+pd98059组p-E RK表达水平明显低于CXCL1组,pd98060组p-ERK表达水平明显低于CXCL1+pd98059组(P<0.01).随着趋化因子CXCL1作用时间的延长,ETS-1、MMP-2蛋白表达水平明显增加(P<0.05).CXCL1组ETS-1、MMP-2表达水平明显高于对照组,CXCL1+pd98059组ETS-1、MMP-2表达水平明显低于CXCL1组,pd98060组ETS-1、MMP-2表达水平明显低于CXCL1+pd98059组(P<0.01).结论趋化因子CXCL1可通过ERK信号通路提升ETS-1、MMP-2蛋白表达水平,促进人宫颈癌细胞的增殖、迁移和侵袭.Objective To investigate the effect of chemokine CXCL1 on the activity of human cervical cancer cells and its molecular mechanism.Method Human cervical cancer cell line C33A was cultured in vitro and divided into control group(conventional medium),CXCL1 group(25,50,100 ng/mL),pd98060 group(100μmol/L pd98060),CXCL1+pd98060 group(100 ng/mL CXCL1+100μmol/L pd98060).MTT assay was used to detect cell proliferation,scratch test and Transwell invasion test were used to detect cell migration and invasion;Western blot was used to detect the expression of phosphorylated extracellular signal regulated kinase(p-ERK),extra-cellular signal regulated kinase(ERK),E26 transcription factor protein 1(ETS-1)and matrix metalloproteinase 2(MMP-2).Results The proliferation level,proliferation rate and invasion rate of cervical cancer cells in CXCL1 group were significantly higher than those in control group(P<0.01);CXCL1 promoted the proliferation,migration and invasion of cervical cancer cells in a concentration dependent manner;The proliferation level,proliferation rate and invasion rate of cervical cancer cells in CXCL1+pd98059 group were significantly lower than those in CXCL1(100 ng/mL)(P<0.01);The proliferation level,proliferation rate and invasion rate of cervical cancer cells in pd98060 group were significantly lower than those in CXCL1+pd98059 group(P<0.01).The expression of p-ERK protein increased significantly with the time of CXCL1(P<0.01).The expression level of p-ERK in CXCL1 group was significantly higher than that in control group,the expression level of p-ERK in CXCL1+pd98059 group was significantly lower than that in CXCL1 group,and the expression level of p-ERK in pd98060 group was significantly lower than that in CXCL1+pdD98059 group(P<0.01).The expression levels of ETS-1 and MMP-2 increased significantly with the prolongation of CXCL1(P<0.05).The expression levels of ETS-1 and MMP-2 in CXCL1 group were significantly higher than those in control group.The expression levels of ETS-1 and MMP-2 in CXCL1+pd98059 group

关 键 词：人宫颈癌细胞 趋化因子CXCL1 细胞外信号调节激酶 E26转录因子1 基质金属蛋白酶2 

分 类 号：R737[医药卫生—肿瘤]