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

Journal Article · Wed Feb 01 04:00:00 EST 2006 · International Journal of Radiation Oncology, Biology and Physics

DOI:https://doi.org/10.1016/J.IJROBP.2005.1· OSTI ID:20793320

Chen, M -F ^[1]; Keng, Peter C ^[2]; Hungyi, Shau ^[3]; Wu, C -T ^[4]; Hu, Y -C ^[5]; Liao, S -K ^[4]; Chen, W -C ^[1]

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1. Department of Radiation Oncology, Chang Gung Memorial Hospital, Taipei, Taiwan (China)
2. Department of Radiation Oncology, University of Rochester School of Medicine and Dentistry, Rochester, New York (United States)
3. Department of Pathology and Laboratory Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY (United States)
4. Graduate Institute of Clinical Medical Sciences, Chang Gung University, Taipei, Taiwan (China)
5. Division of Surgical Oncology, University of California, Los Angeles, David Geffen School of Medicine, Los Angeles, CA (United States)

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.

• OSTI ID: 20793320
• Journal Information: International Journal of Radiation Oncology, Biology and Physics, Journal Name: International Journal of Radiation Oncology, Biology and Physics Journal Issue: 2 Vol. 64; ISSN IOBPD3; ISSN 0360-3016
• Country of Publication: United States
• Language: English

Related Subjects

62 RADIOLOGY AND NUCLEAR MEDICINE
CARCINOMAS
GROWTH
IN VITRO
IN VIVO
LUNGS
METASTASES
MICE
PATIENTS
PROTEINS
RADIOSENSITIVITY
RADIOTHERAPY
TUMOR CELLS