Propofol inhibition of hepatocellular carcinoma via the prevention of reactive oxygen species-induced Cav1 and HO-1 activation
In this study, we showed that Propofol could effectively suppressed the growth of tumor and metastasis derived from metastatic HCC cells, and the growth of HCC patient-derived xenograft. Secondly, we delineated the effect of reactive oxygenase species (ROS) in the activation of Src/caveolin-1 (Cav1). The ROS-induced Cav1 resulted in the upregulation and nuclear translocation of heme oxygenase 1 (HO-1), resulting in HCC aggressive properties. Thirdly, we demonstrated the effect of Propofol in upregulation of mitochondrial antioxidant capacity and suppression of Cav1 expression as well as HO-1 activation in HCC cells. Lastly, we showed that Propofol did not affect the growth of normal hepatocyte, and the exclusive expression of Cav1 and HO-1 in metastatic HCC cells. These findings implicate the potential to develop anti-Cav1 and anti-HO-1 reagents without adverse effects on normal hepatocytes as a new strategy for treating HCC.