FIGURE 10.
Proposed model for the effect of NOX1 on autocrine cell growth of liver tumor cells. Upon serum withdrawal, early ROS production by NOX1 activates an Src/ERK pathway promoting a positive feedback loop on NOX1 up-regulation. In parallel, NOX1-produced ROS stimulate p38 and AKT activation which, in turn, induce TGF-α and EGFR expression and consequently the activation of the EGFR pathway to induce cell growth. This pathway might be common to tumoral liver cells, being inactive in normal cells.