Epidermal growth factor upregulates motility of Mat-LyLu rat prostate cancer cells partially via voltage-gated Na+ channel activity

J Cell Physiol. 2008 Apr;215(1):77-81. doi: 10.1002/jcp.21289.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Movement / drug effects*
  • Epidermal Growth Factor / pharmacology*
  • Ion Channel Gating / drug effects*
  • Male
  • Prostatic Neoplasms / pathology*
  • Quinazolines
  • Rats
  • Sodium Channels / metabolism*
  • Tetrodotoxin / pharmacology
  • Tyrphostins / pharmacology
  • Up-Regulation / drug effects*

Substances

  • Quinazolines
  • Sodium Channels
  • Tyrphostins
  • RTKI cpd
  • Tetrodotoxin
  • Epidermal Growth Factor