Antisense of human peroxiredoxin II enhances radiation-induced cell death

Human peroxiredoxin II (Prx II) has been known to function as an antioxidan t enzyme in cells, Using head-and-neck cancer cell lines, we investigated w hether Prx II expression is related to the resistance of cells to radiation therapy in vivo and in vitro, and whether a Prx II antisense serves as a r adiosensitizer. Increased expression of Prx II was observed in tissues isol ated from the patients who did not respond to radiation therapy, whereas Pr x II expression was weak in tissues from the patients with regressed tumors . Enhanced expression of Prx II in UMSCC-11A (11A) cells was also observed after treatment with gamma radiation. This increased expression conferred r adiation resistance to cancer cells because overexpression of Prx II protec ted 11A cells from radiation-induced cell death, suggesting that blocking P rx II expression could enhance radiation sensitivity. Treatment of 11A cell s with a Prx II antisense decreased induction of Prx II, enhancing the radi ation sensitivity. From these results, we suggest that stress-induced overe xpression of Prx II increases radiation resistance via protection of cancer cells from radiation-induced oxidative cytolysis and that a Prx II antisen se ran be used as a radiosensitizer.