Inhibition of lung tumor growth and augmentation of radiosensitivity by decreasing peroxiredoxin I expression

Miao Fen Chen, Peter C. Keng, Hungyi Shau, Chun Te Wu, Yueh Chiang Hu, Shuen Kuei Liao, Wen Cheng Chen*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

82 Scopus citations


Purpose: In this study, we examined the role of peroxiredoxin I (Prx I) in lung cancer cell growth in vitro and in vivo and its influence on these tumor cells' sensitivity to radiotherapy. Methods and materials: We established stable transfectants of A549 (p53+) and H1299 (p53-) lung carcinoma cell lines with Prx I antisense to downregulate their Prx I protein. We then examined their in vitro biologic changes and used nude mice xenografts of these cell lines to compare tumor invasion, spontaneous metastatic capacity, and sensitivity to radiotherapy. Results: The Prx I antisense transfectants of both cell lines showed a significant reduction in Prx I protein production. Prx I antisense transfectants grew more slowly than did the wild type. As xenografts in mice, A549 Prx I antisense transfectants showed a threefold delay in the generation of palpable tumors. The incidence of spontaneous metastasis of Prx I antisense transfectants was significantly less than that of the wild-type cells. Furthermore, irradiation of Prx I antisense transfectants caused more than twice the growth delay compared with the wild type. Conclusion: The results of these studies suggest that inactivation of Prx I may be a promising approach to improve the treatment outcome of patients with lung cancer.

Original languageEnglish
Pages (from-to)581-591
Number of pages11
JournalInternational Journal of Radiation Oncology Biology Physics
Issue number2
StatePublished - 01 02 2006
Externally publishedYes


  • Lung tumor cell growth
  • Metastasis
  • Peroxiredoxin I
  • Radiation sensitivity


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