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- Publisher
- Wolters Kluwer Health
- Copyright
- Copyright © 2000 American Association for the Study of Liver Diseases
- ISSN
- 0270-9139
- eISSN
- 1527-3350
- DOI
- 10.1053/jhep.2000.17738
- pmid
- 11003625
- Publisher site
- See Article on Publisher Site
Abstract
The Akt/PI‐3 kinase pathway is a system essential for cell survival. In the current study, we showed that hepatocyte growth factor (HGF) activates the Akt/PI‐3 kinase pathway to suppress Fas‐mediated cell death in human hepatocellular carcinoma (HCC; 3 lines; SK‐Hep1, HLE, and Chang Liver cell lines), hepatoblastoma (1 line; HepG2), and embryonic hepatocyte (1 line; WRL). Five tested cell lines showed the resistance to Fas‐mediated cell death by the pretreatment of HGF. This HGF‐induced cell survival was suppressed by wortmannin (Akt/PI‐3 kinase pathway inhibitor), suggesting an involvement of Akt. When cells were pretreated with HGF, Fas‐mediated cell death was suppressed, followed by Akt phosphorylation at Ser473. Fas‐death–inducing signaling complex (DISC) formation, especially FADD and caspase 8 interaction, was suppressed by HGF and the suppression of the Akt/PI‐3 kinase pathway by transient expression of PTEN, resulting in acquisition of Fas‐DISC formation and Fas‐mediated cell death in HGF‐treated cells. We suggest that HGF promotes cell survival in hepatocyte‐derived cell lines (HCC, hepatoblastoma, and embryonic hepatocyte) from Fas‐mediated cell death via Fas‐DISC suppression as a result of Akt activation.
Journal
Hepatology – Wolters Kluwer Health
Published: Oct 1, 2000