Changes in mitochondrial function during EMT induced by TGFβ-1 in pancreatic cancer

Mitochondrial dysfunction is linked to cancer. Differences in the number, morphology and function of mitochondria have been observed between normal cells and cancer cells. However, changes in mitochondrial function during epithelial-mesenchymal transition (EMT) in pancreatic cancer are less known. In the present study, the cultured human pancreatic cancer cell line Panc-1 was treated with transforming growth factor (TGF) beta-1. Mitochondrial functions following TGF beta-1 exposure in pancreatic cancer were investigated. It was noticed that TGF beta-1 treatment induces morphologic changes and a shift from epithelial to mesenchymal phenotype in pancreatic cancer. Furthermore, increased mitochondrial mass was detected in pancreatic cancer following TGF beta-1 treatment. Besides, the production of reactive oxygen species in TGF beta-1-treated pancreatic cancer cells significantly increased compared with the control cells. Our results indicate that the phenomenon of EMT in pancreatic cancer has an association with mitochondrial dysfunction. Mitochondrial dysfunction may be a cause of EMT in pancreatic cancer, which leads to heterogeneity in pancreatic cancer, and may be a potential therapeutic target in the future.