FIG. 8.

Prx I inactivation promotes lung tumor growth in K-ras^G12D-Tg mice. (A) Immunostaining of Prx I, pEKR, cyclin D1, and PCNA in lungs from four groups of mice at 7 months (Scale bars, 50 μm). (B) Quantitation of pERK, cyclin D1, and PCNA-positive cells per tumor area at five different time points at 7 months. The data are presented as the mean±SEM (n=5). ^*p<0.05, ^**p<0.01 compared with WT/K-ras^G12D-Tg mice. (C) Western blots for pERK, cyclin D1, and PCNA 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. (D) Schematic illustration of the expression and function of Prx I in K-ras^G12D-driven lung adenocarcinoma. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/ars