✦ LIBER ✦

Noninvasive methods for the assessment of liver fibrosis: A window open on the future?

✍ Scribed by Massimo Pinzani

Publisher: John Wiley and Sons
Year: 2011
Tongue: English
Weight: 309 KB
Volume: 54
Category: Article
ISSN: 0270-9139
DOI: 10.1002/hep.24584

No coin nor oath required. For personal study only.

✦ Synopsis

The c-Jun NH2-terminal kinase (JNK) signal-transduction pathway has been implicated in the growth of carcinogeninduced hepatocellular carcinoma. However, the mechanism that accounts for JNK-regulated tumor growth is unclear. Here, we demonstrate that compound deficiency of the two ubiquitously expressed JNK isoforms (JNK1 and JNK2) in hepatocytes does not prevent hepatocellular carcinoma development. Indeed, JNK deficiency in hepatocytes increased the tumor burden. In contrast, compound JNK deficiency in hepatocytes and nonparenchymal cells reduced both hepatic inflammation and tumorigenesis. These data indicate that JNK plays a dual role in the development of hepatocellular carcinoma. JNK promotes an inflammatory hepatic environment that supports tumor development, but also functions in hepatocytes to reduce tumor development.

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