Pentraxin-3 (PTX3) is a protein that has a vast array of immune effects including activation of the classical and alternative complement pathways, stimulation of the lectin complement pathway, regulation of leukocyte recruitment, and regulation of inflammatory process. In preliminary (unpublished) studies conducted in mice by Dr. Laurie Shuman Moss, a decreased tumor growth was found to be associated with increased PTX3 expression. In this study, we test if several lines of human lung cancer cells (H322M, H23, A549 and H460) express PTX3 and if PTX3 has a role in epithelial mesenchymal transition (EMT), the change in cell morphology and behavior associated with cancer metastasis. . Cells were treated with varying concentrations of IL-1β, an inducer of PTX3 expression, and TGFβ, a promoter of EMT. In addition to measuring PTX3 expression, Vimentin, E-cadherin and α-smooth muscle actin (α-SMA) gene expression were also measured to evaluate EMT. We found that in the most mesenchymal cell line used in this study, H23, and in the H460 cells line that there was increased PTX3 expression in response to treatment with IL-1β. In the most epithelial cell line used in this study, H322M, and the H460 cell line exhibited increased expression of Vimentin, an EMT marker, in response to TGFβ treatment. This data suggests that the more mesenchymal human lung cancer cell lines can be induced to express PTX3 and that the more epithelial human lung cancer cell lines used were induced to undergo EMT.