Pim-2 Activates API-5 to Inhibit the Apoptosis of Hepatocellular Carcinoma Cells Through NF-κB Pathway |
| |
Authors: | Ke Ren Wei Zhang Yujun Shi Jianping Gong |
| |
Institution: | (1) Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China;(2) West China Hospital of Sichuan University, Chengdu, People’s Republic of China;(3) Department of Hepatobiliary Surgery, The Second College of Clinical Medicine and The Second Affiliated Hospital of Chongqing Medical University, 76# Linjiang Road, Chongqing, 400010, People’s Republic of China; |
| |
Abstract: | Pim-2 is proved to be relevant to the tumorigenesis of hepatocellular carcinoma (HCC), but the mechanism is unclear. We studied
the relationship among Pim-2, NF-κB and API-5. In our experiment, expression level of the three factors and phosphorylation
level of API-5, as well as NF-κB activity, were detected in HCC tissues and the nontumorous controls. Then Pim-2 gene was
transfected into nontumorous liver cells L02, and Pim-2 SiRNA was transfected into hepatoblastoma cell line HepG2. Parthenolide
was added as NF-κB inhibitor. The same detections as above were repeated in the cells, along with the apoptosis analysis.
We found the levels of Pim-2, NF-κB and API-5, as well as NF-κB activity, were significantly higher in HCC tissues. Pim-2
level was increased in L02 cells after the transfection of Pim-2 gene, but decreased in HepG2 cells after the transfection
of Pim-2 SiRNA. The levels of NF-κB and API-5, as well as NF-κB activity and API-5 phosphorylation level, were in accordance
with Pim-2 level, but could be reversed by Parthenolide. Cell apoptosis rates were negatively correlated with API-5 phosphorylation
level. Therefore, we infer that Pim-2 could activate API-5 to inhibit the apoptosis of liver cells, and NF-κB is the key regulator. |
| |
Keywords: | |
本文献已被 SpringerLink 等数据库收录! |
|