Abstract
It is well known that heme oxygenase-1 (HO-1) as well as nitric oxide (NO) synthase expressed in tumor cell line and solid tumor. NO may be beneficial to the tumor growth, not only because enhanced vascular permeability in solid tumor is mediated by NO, but because the l-arginine-dependent NO pathway mediates angiogenic activity and vascular endothelial growth factor (VEGF) induces angiogenesis via formation of NO. However, NO has a powerful cytostatic action on tumor cells by inhibiting DNA synthesis and causing oxidative injury. While it has been suggested that induction of HO-1 may provide an important protective response by cells against oxidative damage, HO-1 expression in tumor cells is strongly enhanced by NO donor. Strong induction of HO-1 is observed in solid tumors after occlusion or embolization of the tumor-feeding artery, indicating that ischemic stress which may involve oxidative stress triggers HO-1 induction. In addition, it is of great importance that an HO inhibitor, zinc protoporphyrin IX, suppressed the tumor growth to a great extent. In conclusion, HO-1 expression in the solid tumor may confer resistance of tumor cells to hypoxic stress as well as to NO-mediated cytotoxicity.
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