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Cell‐adhesion and morphological changes are not sufficient to support anchorage‐dependent cell growth via non‐integrin‐mediated attachment
Author(s) -
Chang HsinHou,
Kau JyhHwa,
Lo Szecheng J,
Sun DerShan
Publication year - 2003
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1016/s1065-6995(02)00295-0
Subject(s) - microbiology and biotechnology , cell adhesion , cell , biology , adhesion , integrin , cell growth , chemistry , biochemistry , organic chemistry
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.