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. 2010 Apr 26;107(19):8788–8793. doi: 10.1073/pnas.1003428107

Fig. 3.

Fig. 3.

Mitochondrial ROS are required for oncogene-induced anchorage-independent growth. (A) Levels of oxidized mito-roGFP in p53DN, Myr-Akt-p53DN, HrasV12-p53DN, and KrasV12-p53DN cells. Mean ± SE (n = 4). *P < 0.05; Statistical comparisons were made between p53DN cells and Myr-Akt, HrasV12, or KrasV12 cells. (B) Intracellular H2O2 levels were assessed by Amplex Red in cell lysates of p53DN, KrasV12-p53DN cells, LSL KrasG12D 3T3 ± Cre. Mean ± SE (n = 4). Data represented is KrasV12-p53DN cells/immortalized p53DN and LSLKrasG12D3T3 +Cre/immortalized LSLKrasG12D. Analysis of soft agar colonies of (C) LSL-Kras G12D, and (D) HCT116 cell lines treated with mitochondrial targeted antioxidants 1 μM MCTPO, 1 μM MCP, or the control compounds 1 μM CTPO, 1 μM CP, and 1 μM TPP. Mean ± SE (n = 9). **P < 0.01; Statistical comparisons are between MCTPO or MCP and TPP.