LPS诱导胰腺癌细胞Panc-1表达B7-H1

LPS induced B7-H1 expression in pancreatic carcinoma Panc-1 cells

目的:研究胰腺癌细胞株Panc-1在应用脂多糖(LPS)刺激前后B7-H1表达的变化,并探讨其可能的分子机制。方法:LPS刺激以及丝裂原活化蛋白激酶(MAPKs)的特异性抑制剂处理Panc-1细胞前后,应用Western blotting检测MAPKs信号通路中p38丝裂原活化蛋白激酶(p38)、细胞外信号调节蛋白激酶(ERK)和c-Jun氨基端激酶(JNK)磷酸化水平的变化,real-time PCR和Western blotting检测B7-H1 mRNA和蛋白的表达变化。结果:LPS刺激后B7-H1的表达显著上调,p38、ERK和JNK的磷酸化水平也明显上调,加入MAPKs特异性的抑制剂后,LPS诱导的p38、ERK和JNK的磷酸化被抑制,并且在p38和ERK的抑制剂处理后,B7-H1的表达也明显被抑制,而在JNK的抑制剂处理后B7-H1的表达没有显著变化。结论:LPS可以诱导胰腺癌细胞株Panc-1表达B7-H1,并且p38和ERK的活化在LPS诱导的B7-H1的表达过程中起着重要作用。

AIM： To explore the mechanism of lipopolysaccharide（LPS）-induced B7-H1 expression in pancreatic carcinoma cell line Panc-1.METHODS： The levels of phosphorylated p38 mitogen-activated protein kinase（p-p38）,phosphorylated extracellular signal-regulated kinase（p-ERK） and phosphorylated c-Jun N-terminal kinase（p-JNK） after stimulated with LPS or treated with mitogen-activated protein kinases（MAPKs） inhibitors were detected by Western blotting.The expression of B7-H1 in Panc-1 cells after LPS stimulation or MAPKs inhibitor treatment was measured by real-time PCR and Western blotting.RESULTS： The levels of B7-H1,p-p38,p-ERK and p-JNK were up-regulated with LPS stimulation.The promoted p-p38,p-ERK and p-JNK levels induced by LPS were inhibited by the corresponding MAPKs inhibitors.Furthermore,the inhibitors of p38 and ERK attenuated LPS-induced B7-H1 expression.However,JNK inhibitor had very little effect on LPS-induced B7-H1 expression.CONCLUSION： LPS induces B7-H1 expression in pancreatic carcinoma cell line Panc-1.ERK and p38 are involved in this regulation as the inhibitors of ERK and p38 attenuate LPS-induced B7-H1 expression.