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. 2013 Aug 10;19(5):482–496. doi: 10.1089/ars.2011.4421

FIG. 7.

FIG. 7.

ROS/ERK pathway involves oncogenic K-ras-driven tumor growth. (A) NCI-H358 cells were transfected with siPrx I and cultured in the presence or absence of U0126 (10 μM) and subjected to CCK-8 cell proliferation assay at the indicated time. The data are representative of at least three different experiments and presented as mean±SEM. ***p<0.001 compared with the cells transfected with siPrx I cultured in U0126, ***p<0.001 compared with the cells transfected with scrambled siRNA cultured in U0126. (B) CCK-8 cell proliferation assay was carried out using K-rasG12D/Prx I−/− 3T3-MEFs cells cultured in the presence or absence of U0126 (10 μM) or PD98059 (20 μM) for 72 h. The data are representative of at least three different experiments and presented as mean±SEM. **p<0.01, ***p<0.001 compared with the cells cultured in DMSO. (C) A549 cells were stably transfected with human Prx I expression vector, and ROS levels were measured by flow cytometry. The data are representative of at least three different experiments and presented as mean±SEM. **p<0.01, ***p<0.001 compared with A549 Mock cells. (D) Anchorage-independent growth assay was performed using stably expressed Prx I in A549 cells. The data are representative of at least three different experiments. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/ars