CXCL12经ERK通路对宫颈癌细胞增殖、侵袭转移的影响及机制

目的:探究趋化因子CXCL12对宫颈癌caski细胞增殖、侵袭和转移的影响及可能的信号通路.方法:体外培养宫颈癌caski细胞株.分对照组、CXCL12组(25、50、100、200 ng/ml)、100 ng/ml CXCL12+100μmol/L PD98059组、(100μmol/L)PD98059组.MTT、细胞划痕实验、Transwell侵袭实验分别检测细胞增殖、转移和侵袭能力的变化;免疫印迹检测细胞外信号调节激酶(ERK)、磷酸化细胞外信号调节激酶(p-ERK)、基质金属蛋白酶2(MMP-2)、E26转录因子蛋白(ETS-1)的表达.结果:CXCL12浓度依赖性促进细胞增殖、黏附、划痕愈合、细胞侵袭增加;100 ng/ml与200 ng/ml之间差异无统计学意义.ERK通路抑制剂PD98059可阻断CXCL12的上述作用.与对照组相比,CXCL12可明显促进p-ERK、ETS-1、MMP-2蛋白表达;与CXCL12组相比,PD98059可显著降低上述蛋白表达.结论:CXCL12可能通过ERK通路影响ETS-1、MMP-2蛋白的表达,促进宫颈癌细胞的增殖、侵袭和转移.

Effect of CXCL12 on proliferation,invasion and metastasis of cervical cancer cells via ERK pathway and its mechanism

Objective :To investigate the effects of chemokine CXCL12 on proliferation,invasion and metastasis of cervical cancer caski cells and possible signaling pathways. Methods :Cervical cancer caski cell line cultured in vitro was divided into control group,CXCL12 group (25,50,100,200 ng/ml),CXCL12+PD98059 group (100 ng/ml CXCL12+100 μmol/L PD98059) and PD98059 group (100 μmol/L). MTT,cell scratch assay and Transwell invasion assay were used to detect the changes of cell proliferation,metastasis and invasion. The expressions of t-ERK, p-ERK,MMP-2 and ETS-1 was detected by Western blotting. Results :CXCL12 concentration-dependently promoted cell proliferation,adhesion,scratch healing and cell invasion. According to the results,it could be observed that the difference between 100 ng/ml and 200 ng/ml was not statistically significant. PD98059 had the capacity to block the above effects of CXCL12. Compared with the control group,CXCL12 promoted the expression of p-ERK,ETS-1, MMP-2 proteins significantly. Compared with the CXCL12 group,PD98059 significantly decreased the above protein expression. Conclusion :CXCL12 may affect the expression of ETS-1 and MMP-2 proteins through ERK pathway and promote the proliferation,invasion and metastasis of cervical cancer cells.