NET1-mediated RhoA activation facilitates lysophosphatidic acid-induced cell migration and invasion in gastric cancer

Br J Cancer. 2008 Oct 21;99(8):1322-9. doi: 10.1038/sj.bjc.6604688. Epub 2008 Sep 30.

Abstract

The most lethal aspects of gastric adenocarcinoma (GA) are its invasive and metastatic properties. This aggressive phenotype remains poorly understood. We have recently identified neuroepithelial cell transforming gene 1 (NET1), a guanine exchange factor (GEF), as a novel GA-associated gene. Neuroepithelial cell transforming gene 1 expression is enhanced in GA and it is of functional importance in cell invasion. In this study, we demonstrate the activity of NET1 in driving cytoskeletal rearrangement, a key pathological mechanism in gastric tumour cell migration and invasion. Neuroepithelial cell transforming gene 1 expression was increased 10-fold in response to treatment with lysophosphatidic acid (LPA), resulting in an increase in active levels of RhoA and a 2-fold increase in cell invasion. Lysophosphatidic acid-induced cell invasion and migration were significantly inhibited using either NET1 siRNA or a RhoA inhibitor (C3 exoenzyme), thus indicating the activity of both NET1 and RhoA in gastric cancer progression. Furthermore, LPA-induced invasion and migration were also significantly reduced in the presence of cytochalasin D, an inhibitor of cytoskeletal rearrangements. Neuroepithelial cell transforming gene 1 knockdown resulted in AGS cell rounding and a loss of actin filament organisation, demonstrating the function of NET1 in actin organisation. These data highlight the importance of NET1 as a driver of tumour cell invasion, an activity mediated by RhoA activation and cytoskeletal reorganisation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / metabolism*
  • Adenocarcinoma / pathology
  • Blotting, Western
  • Cell Line, Tumor
  • Cell Movement / physiology
  • Cytoskeletal Proteins / drug effects
  • Cytoskeletal Proteins / metabolism
  • Cytoskeleton / drug effects
  • Cytoskeleton / metabolism
  • Cytoskeleton / pathology
  • Enzyme Activation / drug effects
  • Enzyme Activation / physiology
  • Flow Cytometry
  • Gene Expression
  • Humans
  • Lysophospholipids / pharmacology*
  • Neoplasm Invasiveness / physiopathology*
  • Oncogene Proteins / genetics
  • Oncogene Proteins / metabolism*
  • Polymerase Chain Reaction
  • RNA Interference
  • RNA, Messenger / analysis
  • Stomach Neoplasms / metabolism*
  • Stomach Neoplasms / pathology
  • rhoA GTP-Binding Protein / drug effects
  • rhoA GTP-Binding Protein / metabolism*

Substances

  • Cytoskeletal Proteins
  • Lysophospholipids
  • NET1 protein, human
  • Oncogene Proteins
  • RNA, Messenger
  • RHOA protein, human
  • rhoA GTP-Binding Protein
  • lysophosphatidic acid