Influence of
PKB on ROS Regulation of Proliferation in Human 7721 Hepatoma Cells
LIU Shan-Lin*, LIU Guan-Zhong,
CHENG Jian, SHI Dong-Yun, CHEN Hui-Li, ZHANG Ya-Dong
( Department of Biochemistry, Medical Center of Fudan University, Shanghai 200032, China )
Abstract In the
present study, the relationship
between PKB signaling and reactive oxygen species (ROS) during the course of
exogenous and endogenous ROS orantioxidants regulating human 7721 hepatoma cell
proliferation was studied. Tochange 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
μmol/L) significantly stimulated PKB activity and c-fos/c-jun
expression and cell growth, which could be abolishedby 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; thePKB 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.
Key words PKB; ROS; antioxidant; AP-1; hepatoma cell
*Corresponding author: Tel,
021-64041900-2698; e-mail, [email protected]