| Autor: |
Liu SL; Department of Biochemistry, Medical Center of Fudan University, Shanghai 200032, China. slliu@shmu.edu.cn, Liu GZ, Cheng J, Shi DY, Chen HL, Zhang YD |
| Jazyk: |
čínština |
| Zdroj: |
Sheng wu hua xue yu sheng wu wu li xue bao Acta biochimica et biophysica Sinica [Sheng Wu Hua Xue Yu Sheng Wu Wu Li Xue Bao (Shanghai)] 2002 Jan; Vol. 34 (1), pp. 67-72. |
| Abstrakt: |
In the present study, the relationship between PKB signaling and reactive oxygen species (ROS) during the course of exogenous and endogenous ROS or antioxidants regulating human 7721 hepatoma cell proliferation was studied. To change endogenous ROS levels, 7721 cells were transfected with human manganese superoxide dismutase (MnSOD) construct containing sense or antisense MnSOD cDNA. Low level of exogenous ROS H2O2(1-10 mumol/L) significantly stimulated PKB activity and c-fos/c-jun expression and cell growth, which could be abolished by antioxidant danshensu (40 mg/L). It was observed that overexpression of MnSOD inhibited 7721 cell growth by inhibiting PKB activity and c-fos/c-jun expression; the PKB activity and c-fos/c-jun expression, however, were stimulated by down-regulated MnSOD expression. In addition, PKB-7721 cells (transfected with sense PKB cDNA) promoted c-fos/c-jun expression by stimulating PKB activity. These results suggest that the redox state stimulated hepatoma cell growth through PKB pathway, which modulates AP-1 expression. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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