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Aquaporin (AQP) water channels are expressed in high-grade tumor cells ofdifferent tissue origins. In this study, we investigated whether AQP3 is expressedin cultured MPC-83 pancreatic cancer cells, whether AQP3 enhances cell migrationand the signal pathway mechanism involved. MPC-83 pancreatic cancer cells werepre-treated and treated with EGF at different time points and then analyzed usingwestern blotting. Results showed that epidermal growth factor (EGF) induced thephosphorylation of the EGF receptor (EGFR) and extracellular signal-regulatedkinase (ERK), which peaked at 5 min after EGF treatment. EGFR and ERK phosphorylationinduced by EGF were inhibited by PD153035 (EGFR tyrosine kinase inhibitor) andU0126 (ERK inhibitor), respectively. EGF increased the activity of AQP3 in a dose-and time-dependent manner in MPC-83 pancreatic cancer cells, which peaked at 24 hafter treatment. The activity of AQP3 and cell migration were inhibited by PD153035,U0126 and CuSO4 (AQP3 water transport inhibitor). EGFR/ERK pathway-mediated AQP3activation and cell migration were stimulated by EGF in cultured MPC-83 pancreaticcancer cells in vitro and this cell signaling pathway is inhibited by the EGFRand ERK inhibitors, which may be used as potential therapeutic targets in thetreatment of pancreatic cancer.

Epidermal growth factor enhances MPC-83 pancreatic cancer cell migration through the upregulation of aquaporin 3