FIG. 3.

Acceleration of lung tumorigenesis in Prx I^−/−/K-ras^G12D-Tg mice. (A) Schematic diagram of the breeding strategy. WT/K-ras^G12D-Tg and Prx I^−/−/K-ras^G12D-Tg mice were obtained by crossing B6129F1 (C57BL6/J×129/svj) mice carrying the K-ras^G12D and Prx I^−/− alleles. (B) Genotyping of NTg, WT/K-ras^G12D-Tg, Prx I^−/−, and Prx I^−/−/K-ras^G12D-Tg mice by PCR experiments. The littermates served as NTg controls in all the experiments. (C) H&E stained sections of typical lesions in lungs from four groups of mice at 9 weeks (Scale bars, 50 μm). Tumors are indicated by black arrows and white asterisks. Bottom panel is a low-magnification image of WT/K-ras^G12D-Tg and Prx I^−/−/K-ras^G12D-Tg mice. Insets show representative histology in high magnification. Tumor number (D) and tumor size (E) in lungs from WT (n=10), WT/K-ras^G12D-Tg (n=8), Prx I^−/− (n=10), and Prx I^−/−/K-ras^G12D-Tg (n=11) mice at 9 weeks. The data are presented as mean±SEM. ^**p<0.01, ^***p<0.001 compared with WT/K-ras^G12D-Tg mice. (F) Western blots for K-ras, Prx I, Nrf2, Keap1, and HO-1 in lungs from WT (n=2), Prx I^−/− (n=2), WT/K-ras^G12D-Tg (n=2), and Prx I^−/−/K-ras^G12D-Tg (n=3) mice at 7 months. WT, wild type. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/ars