| First Author | Wang AG | Year | 2011 |
| Journal | Biochem Biophys Res Commun | Volume | 409 |
| Issue | 3 | Pages | 532-8 |
| PubMed ID | 21600874 | Mgi Jnum | J:174082 |
| Mgi Id | MGI:5051868 | Doi | 10.1016/j.bbrc.2011.05.039 |
| Citation | Wang AG, et al. (2011) Steatosis induced by the accumulation of apolipoprotein A-I and elevated ROS levels in H-ras12V transgenic mice contributes to hepatic lesions. Biochem Biophys Res Commun 409(3):532-8 |
| abstractText | Hepatic steatosis is considered to have an important impact on liver tumorigenesis, despite a lack of clear experimental evidence. Histopathological analysis of H-ras12V transgenic mice showed liver lesions on a steatosis background had significantly higher incidence than on a non-steatosis background. Further investigation showed that apolipoprotein A-I was elevated and accumulated around fatty vacuoles. This elevated level of apolipoprotein A-I was coupled with an elevated level of H-ras12V protein and ROS. In conclusion, our results suggest that the expression of H-ras12V oncogene leads to elevated levels of ROS and apolipoprotein A-I that contribute to steatosis. The steatosis, in turn, promotes the development of hepatic lesions induced by H-ras12V oncogene. |
