Antisense of human peroxiredoxin II enhances radiation-induced cell death

Sun Hee Park, Young Min Chung, Yong Sik Lee, Hyung Jung Kim, Jun Suk Kim, Ho Zoon Chae, Young Do Yoo

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Abstract

Human peroxiredoxin II (Prx II) has been known to function as an antioxidant enzyme in cells. Using head-and-neck cancer cell lines, we investigated whether 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 radiosensitizer. Increased expression of Prx II was observed in tissues isolated from the patients who did not respond to radiation therapy, whereas Prx 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 γ radiation. This increased expression conferred radiation resistance to cancer cells because overexpression of Prx II protected 11A cells from radiation-induced cell death, suggesting that blocking Prx II expression could enhance radiation sensitivity. Treatment of 11A cells with a Prx II antisense decreased induction of Prx II, enhancing the radiation sensitivity. From these results, we suggest that stress-induced overexpression of Prx II increases radiation resistance via protection of cancer cells from radiation-induced oxidative cytolysis and that a Prx II antisense can be used as a radiosensitizer.

Original languageEnglish
Pages (from-to)4915-4920
Number of pages6
JournalClinical Cancer Research
Volume6
Issue number12
Publication statusPublished - 2000

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ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Park, S. H., Chung, Y. M., Lee, Y. S., Kim, H. J., Kim, J. S., Chae, H. Z., & Yoo, Y. D. (2000). Antisense of human peroxiredoxin II enhances radiation-induced cell death. Clinical Cancer Research, 6(12), 4915-4920.