Work

The role of JNK in the development of hepatocellular carcinoma

Year: 2011

Type: preprint

Abstract: The cJun NH(2)-terminal kinase (JNK) signal transduction pathway has been implicated in the growth of carcinogen-induced 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.

Source: Genes & Development

DOI: 10.1101/gad.1989311

Authors: Madhumita Das, David S. Garlick, Dale L. Greiner, Roger J. Davis

Institutions: University of Massachusetts Chan Medical School, Howard Hughes Medical Institute

Language: English

Topic: Liver physiology and pathology

Subfield: Hepatology

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: green