Macrophage phenotypes influence lung cancer migration (P2221)

Abstract

Background: Lung cancer is the leading cause of cancer mortality. Studies have demonstrated that high macrophage density correlated with high microvessicle density and poor patient prognosis. Tumor associated macrophage are believed to predominantly possess an alternatively activated phenotype (M2). Hallmarks of this population include pro-angiogenesis, wound repair and extracellular matrix degradation. We investigated the role macrophage play in lung cancer migration. Methods: Human lung cancer lines A549, H1299, H1792, H1975 & H1650 were used. Murine bone marrow differentiated macrophages were stimulated with IFN-γ or IL-4 to achieve classically activated (M1) and M2 populations. Conditioned media (24 h) was collected and used in migration assays. Migration was assessed using BD 24 well FluoroBlok cell culture inserts. Results: qRT-PCR showed that stimulated M1 had a 344 fold increase (p<0.01) of iNos and stimulated M2 had a 39 fold increase (p<0.01) in Arg-1. Migration increased 20% (p<0.01) in A549 cells when cultured in M2 conditioned media. However, when macrophage and lung cancer cells were co-culture, migration of H1299 and H1650 increased by 82% (p<0.01) and 184% (p<0.01) respectively. Conclusions: Our studies suggest that macrophage produce cytokines that influence the migratory abilities of lung cancer cell lines.