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. Author manuscript; available in PMC: 2010 Mar 15.
Published in final edited form as: Cancer Res. 2009 Mar 10;69(6):2375–2383. doi: 10.1158/0008-5472.CAN-08-3359

Figure 1.

Figure 1

Biochemical characterization of mitochondria dysfunction of H and P clone cells. A, schematic representation of the establishment of MCF7 subclones. Cells were treated for 24 h with rotenone (100 nmol/L), which caused an increase in superoxide generation, as measured by flow cytometry (left ; numbers indicate the mean superoxide values). Cells were then cultured in drug-free medium for 48 h, followed by two more cycles of rotenone treatment. Cells were then plated at a density of 200 per dish and colonies were isolated. B, comparison of ROS generation by parental MCF7 cells and its subclones (H and P clones) using 3 µmol/L CM-H2DCF-DA measured by flow cytometry. C, comparison of oxygen consumption (left ), glucose uptake (center), and lactate production (right) in MCF7 cells and subclones. Columns, mean of three independent experiments; bars, SD. D, comparison of mitochondrial mass (left ), mitochondrial transmembrane potential (Δψm; center), and cell growth (right ) of MCF7 cells and subclones. Results of a representative experiment (n = 3).