Mechanism Of LPS Induced B7-H1Expression On Pancreatic Carcinoma Panc-1Cells

ObjectiveTo explore the mechanism of lipopolysaccharide (LPS) induced B7-H1expression on pancreatic carcinoma cell line Panc-1.Methodsphosphorylation-p38mitogen-activated protein kinase (p-p38), phosphorylation-extracellular signal-regulated kinases (p-ERK) and phosphorylation-c-Jun N-terminal kinase (p-JNK) level after LPS stimulation or Mitogen-activated protein kinases(MAPKs) inhibitors treatment were detected by Western-blotting. The expression of B7-H1on Panc-1cells after LPS stimulation or MAPKs inhibitors treatment was measured by real-time PCR and Western-blotting.ResultsThe level of B7-H1, p-p38. p-ERK and p-JNK was up-regulated with LPS stimulation. The promoted p-p38, p-ERK and p-JNK level induced by LPS could be inhibited with corresponding MAPKs inhibitors respectively. Furthermore, p38and ERK inhibitors could attenuate LPS induced B7-H1expression. Meanwhile, JNK inhibitor had very little effect on LPS induced B7-H1expression. ConclusionLPS could induce B7-H1expression in pancreatic carcinoma cell line Panc-1. ERK and p38were involved in this regulation as ERK and p38inhibitors could attenuate LPS induce B7-H1expression.