Cell-adhesion and morphological changes are not sufficient to support anchorage-dependent cell growth via non-integrin-mediated attachment

Hsin Hou Chang*, Jyh Hwa Kau, Szecheng J. Lo, Der Shan Sun

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

11 Scopus citations

Abstract

Cell-adhesion and spread are important for cell survival. Although extensive studies have suggested several potential mechanisms of action, it is not yet clear how important cell-morphological change per se contributes to the cell-surviving signal. We employed a non-integrin-mediated cell-adhesion system to explore this question. BHK-Japanese encephalitis virus (JEV) cells (BHK21 cells that are persistently infected with JEV) express a large amount of JEV-envelope protein (JEV E) on their surfaces, and can attach and form pseudopodia on the anti-JEV E antibody-coated substrates. However, cells that adhered on the antibody substrate underwent a caspase-3-mediated apoptosis together with a down-regulation of mitogen-activated protein kinase activity within 20 h after adhesion, which indicates that viral-protein-mediated cell-adhesion and cell-spread are not sufficient for supporting cell survival. This provides a different perspective for the study of the relationships between the cell-morphological change and the cell-survival signal.

Original languageEnglish
Pages (from-to)123-133
Number of pages11
JournalCell Biology International
Volume27
Issue number2
DOIs
StatePublished - 01 02 2003
Externally publishedYes

Keywords

  • Caspase-3
  • Cell-adhesion
  • Cell-death
  • Japanese encephalitis virus-persistent cell
  • Mitogen-activated protein kinase
  • Rhodostomin

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