Abnormal expression of
aquaporins (AQPs) has been reported in several human
cancers.
Epidermal growth factor receptor (EGFR)-extracellular signal-regulated kinases1/2 (ERK1/2) are associated with
tumorigenesis and
cancer progression and may upregulate AQPs expression. In this study, we investigated acquaporin-8 expression and signaling via
epidermal growth factor receptor-extracellular signal-regulated kinases1/2 in human
esophageal cancer Eca-109 cells by western blot, immunofluorescence and wound healing (scratch) assays. Our results showed that
epidermal growth factor (
EGF) induced both Eca-109 migration and AQP8 expression. Wound healing results showed that cell migration was increased by 1.23-1.10-fold at 24 h and 48 h after
EGF treatment. AQP8 expression was significantly increased (1.19-fold) at 48 h after
EGF treatment in Eca-109. The EGFR
kinase inhibitor,
PD153035, blocked
EGF-induced AQP8 expression and cell migration. AQP8 expression was decreased from 3.65-fold (
EGF-treated) to 0.55-fold (PD153035-treated) in Eca-109. Furthermore, the
MEK [MAPK (
mitogen-activated protein kinase)/Erk1/2]/Erk1/2 inhibitor
U0126 also inhibited
EGF-induced AQP8 expression and cell migration. AQP8 expression was decreased from 3.92-fold (
EGF-treated) to 1.38-fold (U0126-treated) in Eca-109. In conclusions,
EGF induces AQP8 expression and cell migration in Eca-109 cells via the EGFR/Erk1/2 signal transduction pathway.