Epidermal growth factor upregulates motility of Mat-LyLu rat prostate cancer cells partially via voltage-gated Na+ channel activity.
The main aim of this investigation was to determine whether a functional relationship existed between epidermal growth factor (EGF) and voltage-gated sodium channel (VGSC) upregulation, both associated with strongly metastatic prostate cancer cells. Incubation with EGF for 24 h more than doubled VGSC current density. Similar treatment with EGF significantly and dose-dependently enhanced the cells' migration through Transwell filters. Both the patch clamp recordings and the migration assay suggested that endogenous EGF played a similar role. Importantly, co-application of EGF and tetrodotoxin, a highly selective VGSC blocker, abolished 65% of the potentiating effect of EGF. It is suggested that a significant portion of the EGF-induced enhancement of migration occurred via VGSC activity.
Ding
Yanning
Y
Neuroscience Solutions to Cancer Research Group, Division of Cell and Molecular Biology, Imperial College London, South Kensington Campus, London, UK.
Brackenbury
William J
WJ
Onganer
Pinar U
PU
Montano
Ximena
X
Porter
Louise M
LM
Bates
Lucy F
LF
Djamgoz
Mustafa B A
MB
D000818:Animals; D002465:Cell Movement / Q000187:drug effects*; D004815:Epidermal Growth Factor / Q000494:pharmacology*; D015640:Ion Channel Gating / Q000187:drug effects*; D008297:Male; D011471:Prostatic Neoplasms / Q000473:pathology*; D011799:Quinazolines; D051381:Rats; D015222:Sodium Channels / Q000378:metabolism*; D013779:Tetrodotoxin / Q000494:pharmacology; D020032:Tyrphostins / Q000494:pharmacology; D015854:Up-Regulation / Q000187:drug effects*
D011799:Quinazolines; D015222:Sodium Channels; D020032:Tyrphostins; C101044:RTKI cpd; D013779:Tetrodotoxin; D004815:Epidermal Growth Factor