Document Type
Journal ArticlePublication Date
2011-03-15Keywords
AnimalsCarcinoma, Hepatocellular
Cell Proliferation
Cyclin-Dependent Kinase Inhibitor p21
Cytokines
*Hepatocytes
Interleukin-6
Liver
Liver Neoplasms
Liver Regeneration
Mice
Mice, Inbred C57BL
*Mitogen-Activated Protein Kinase 8
Mitogen-Activated Protein Kinase 9
Proto-Oncogene Proteins c-myc
Signal Transduction
Tumor Cells, Cultured
JNK
partial hepatectomy
hepatocellular carcinoma
Biochemistry
Cancer Biology
Cell Biology
Cellular and Molecular Physiology
Developmental Biology
Molecular Biology
Metadata
Show full item recordAbstract
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 Dev. 2011 Mar 15;25(6):634-45. doi: 10.1101/gad.1989311. Link to article on publisher's site
DOI
10.1101/gad.1989311Permanent Link to this Item
http://hdl.handle.net/20.500.14038/28303PubMed ID
21406557Related Resources
Rights
Copyright © 2011 by Cold Spring Harbor Laboratory Press. Freely available online through the Genes and Development Open Access option.ae974a485f413a2113503eed53cd6c53
10.1101/gad.1989311