志賀 智子
   Department   School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine
   Position   Associate Professor
Article types Original article
Language English
Peer review Non peer reviewed
Title Cell adhesion aside from integrin system can abrogate anoikis in rat liver cells by down-regulation of FasL expression, not by activation of PI-3K/Akt and ERK signaling pathway.
Journal Formal name:Biochemical and biophysical research communications
Abbreviation:Biochem Biophys Res Commun
ISSN code:(0006-291X)0006-291X(Linking)
Domestic / ForeginForegin
Volume, Issue, Page 300(1),pp.201-8
Author and coauthor Ishida Koji†, Nagahara Hikaru, Kogiso Tomomi, Aso Tomoko, Hayashi Naoaki, Akaike Toshihiro
Publication date 2003/01
Summary Epithelial cells require contact with extracellular matrix (ECM) to inhibit detachment-induced apoptosis (anoikis). The ERK and PI-3K/Akt signaling pathways have been identified to inhibit anoikis. We present here a different story. An adult rat liver cell line, ARLJ301-3, underwent apoptosis within 4h under suspension conditions even with active forms of Akt and ERK1/2. Once ARLJ301-3 cells are plated on tissue culture plates coated with synthetic polymer, such as poly-(N-p-vinyl benzyl-O-beta-D-galactopyranosyl-D-gluconamide) (PVLA), poly-L-lysine or polystyrene, instead of functional ECM such as fibronectin, they could survive and proliferate without activation of Akt and ERK1/2. The expression of Fas receptor ligand (FasL) is specifically detected in cells under suspension conditions or treated with cytochalasin-D. We present here the first report that FasL expression is up-regulated by the cytoskeletal disruption directed by cytochalasin-D treatment or cell detachment from ECM.
DOI org/10.1016/S0006-291X(02)02790-0
PMID 12480544