Objective:To explore the influence of motif chemokine ligand 7(CCL7) on pancreatic cell migration and invasion under hypoxic condition.Methods:We isolated cancer-associated pancreatic stellate cells(PSCs) by an outgrowth method,and analyzed the difference of chemokine expression in PSCs between hypoxia (1%) and normoxia (21%) by conducting a chemokine antibody array.By adding different concentration of recombinant protein CCL7(0 ng/mL,1 ng/mL,10 ng/mL,100 ng/mL) to the lower chamber containing 0.1% FBS DMEM,cell invasion assays were performed to determine the dose-dependent manner between CCL7 and invasion of pancreatic ancer cell(PCCs).By conducting Transwell invasion assays and lentiviral transfection,we were able to show that hypoxia induced secretion of CCL7 in PSCs,leading to increased invasion of PSCs.Results:Conditioned media from hypoxic PSCs enhanced PCCs invasiveness more intensely than that from normoxic PSCs(P＜0.05).Among various chemokiness,which were related to invasiveness,CCL7 was one of the overexpressed molecules in supernatant of hypoxic PSCs.CCL7 recombinant protein(0 ng/mL,1 ng/mL,10 ng/mL,100 ng/mL) induced pancreatic cells migration in dose-dependent manner.Pancreatic cells were shown to express CCR5 receptors for CCL7 detected by flow cytometry(P＜0.05).PSCs(Miapaca-2,colo357),which were chultured with PSCs supernatant,were involved an epithelial mesenchymal transition(EMT)cascade.Furthermore,the inbition of CCL7 by lentiviral transfecton suppressed the EMT.Conclusion:Hypoxic stellate cells of pancreatic cancer stroma induce PCCs invasion vis CCL7/CCR5 axis,of which the mechanism might inclued an epithelial mesenchymal transition (EMT) process.