Conclusion: These findings demonstrate the oncogenic potential of TRAF6 during hepatocarcinogenesis by modulating TRAF6/HDAC3/c-Myc signaling, with potential implications for HCC therapy.
Blocking cholesterol synthesis via the dominant negative form of Srebp2 (<i>dnSrebp2</i>) completely prevented sgPten/c-Met-driven hepatocarcinogenesis in <i>Fasn</i> knockout mice.
PTEN plays a key role in hepatocarcinogenesis and reduction of PTEN expression is related to increased expression of CD133, EpCAM and CK19, which is a useful tool to evaluate HCC prognosis and recurrence.
Furthermore, DEN and high-fat diet (HFD)-induced liver carcinogenesis was reduced in <i>TKT<sup>flox/flox</sup>Alb-Cre</i> mice compared with control littermates.
Although there are associations among oxidative stress, reduced nicotinamide adenine dinucleotide phosphate oxidase (NOX) activation, and hepatocellular carcinoma (HCC) development, it is not clear how NOX contributes to hepatocarcinogenesis.
Therefore, the dowregulation of SLU7 and the alterations of this pathway that we observe in the cirrhotic liver could be involved in the process of hepatocarcinogenesis.
Lastly, in the transgenic mouse model of HCC, absence of TLR3 expression was accompanied by a lower rate of preneoplastic hepatocyte apoptosis and accelerated hepatocarcinogenesis without altering the tumor immune infiltrate.
Here, we analyzed the functional relevance of SNAI1 in promoting hepatocarcinogenesis in the context of the AKT/c-Met-driven mouse liver tumor model (AKT/c-Met/SNAI1).
In this study, for hepatocarcinogenesis, wild-type (WT), PRDX4 knockout (PRDX4<sup>-/y</sup>), and human PRDX4 transgenic (hPRDX4<sup>+/+</sup>) mice were given a weekly intraperitoneal injection of diethylnitrosamine for 25 weeks.
Decades of study have utilized the <i>Mat1a</i>-knockout (KO) mouse that spontaneously develops non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC) to elucidate a variety of mechanisms by which MAT proteins dysregulation contributes to liver carcinogenesis.