The molecular regulation of the lung metastasis of pancreatic carcinoma (PCC) is not completely understood. Here, we show that the levels of phosphorylated SMAD3, ZEB1, ZEB2, Snail1, and Snail2 were significantly higher in PCC with lung metastasis than in PCC without lung metastasis. Overexpression of TGF beta 1 enhanced the invasiveness of PCC cells, while inhibition of TGF beta 1 decreased the invasiveness of PCC cells, which appeared to be conducted by activated TGF beta receptor signaling-induced upregulation of ZEB1, ZEB2, Snail1, and Snail2, suggesting a process of epithelial-mesenchymal transition (EMT). Taken together, our study provides evidence that TGF beta receptor signaling-induced EMT may be responsible for the increased PCC invasiveness to enhance its lung metastasis.