Aquaporin (AQP) water channels are expressed in high-grade tumor cells of different tissue origins. In this study, we investigated whether AQP3 is expressed in cultured MPC-83 pancreatic cancer cells, whether AQP3 enhances cell migration and the signal pathway mechanism involved. MPC-83 pancreatic cancer cells were pre-treated and treated with EGF at different time points and then analyzed using western blotting. Results showed that epidermal growth factor (EGF) induced the phosphorylation of the EGF receptor (EGFR) and extracellular signal-regulated kinase (ERK), which peaked at 5 min after EGF treatment. EGFR and ERK phosphorylation induced by EGF were inhibited by PD153035 (EGFR tyrosine kinase inhibitor) and U0126 (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 h after treatment. The activity of AQP3 and cell migration were inhibited by PD153035, U0126 and CuSO4 (AQP3 water transport inhibitor). EGFR/ERK pathway-mediated AQP3 activation and cell migration were stimulated by EGF in cultured MPC-83 pancreatic cancer cells in vitro and this cell signaling pathway is inhibited by the EGFR and ERK inhibitors, which may be used as potential therapeutic targets in the treatment of pancreatic cancer.
Molecular Medicine Reports 06/2012; 6(3):607-10. DOI:10.3892/mmr.2012.966 · 1.48 Impact Factor