志賀 智子
Department School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine Position Associate Professor |
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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 / Foregin | Foregin |
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 |