*How do you stay standing when the ground is torn from beneath your feet?* Becket and Christian are taking the first, tentative steps towards the committed D/s relationship they both crave when the world literally explodes around them. In a frightening reversal of roles, Becket has to deal with his
JNK: A double-edged sword in tumorigenesis
β Scribed by Francisco Javier Cubero; Gang Zhao; Christian Trautwein
- Publisher
- John Wiley and Sons
- Year
- 2011
- Tongue
- English
- Weight
- 309 KB
- Volume
- 54
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
β¦ 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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