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.
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.
Authors: Tatyana A Zykova; Feng Zhu; Tatyana I Vakorina; Jishuai Zhang; Lee Ann Higgins; Darya V Urusova; Ann M Bode; Zigang Dong Journal: J Biol Chem Date: 2010-07-20 Impact factor: 5.157
Authors: Jonah R Riddell; Wiam Bshara; Michael T Moser; Joseph A Spernyak; Barbara A Foster; Sandra O Gollnick Journal: Cancer Res Date: 2011-02-22 Impact factor: 12.701
Authors: Warren Fiskus; Veena Coothankandaswamy; Jianguang Chen; Hongwei Ma; Kyungsoo Ha; Dyana T Saenz; Stephanie S Krieger; Christopher P Mill; Baohua Sun; Peng Huang; Jeffrey S Mumm; Ari M Melnick; Kapil N Bhalla Journal: Cancer Res Date: 2016-08-08 Impact factor: 12.701