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. Author manuscript; available in PMC: 2014 Aug 28.
Published in final edited form as: Cancer Lett. 2013 May 17;337(1):77–89. doi: 10.1016/j.canlet.2013.05.017

Fig. 6.

Fig. 6

Reversal of resistance in rrSUM149 is mediated by enhanced sensitivity toward ROS-mediated cell death. (A) Cytoplasmic superoxides as measured by flow cytometric staining with DHE of (left to right) SUM149 parental cells (white bars) untreated and treated with 7.5 μM lapatinib, rSUM149 cells (black bars) growing in 7.5 μM lapatinib, and rrSUM149 cells following removal of drug for one or two months (gray bars) treated with 7.5 μM lapatinib. (B) Hydrogen peroxide-derived radicals as measured by flow cytometric staining with H2DCFDA in SUM149 parental cells (white bars) untreated and treated with 7.5 μM lapatinib, rSUM149 cells (black bars) growing in 7.5 μM lapatinib, and rrSUM149 cells following removal of drug for one or two months (gray bars) treated with 7.5 μM lapatinib. (C) Western immunoblot analysis of AMPK expression and phosphorylation in rrSUM149 cells treated with 7.5 μM lapatinib following one or two months of growth in lapatinib-free media. (D) Western immunoblot analysis of basal XIAP, cIAP1, cIAP2, survivin, Bcl-2, and Smac expression in untreated SUM149, rSUM149, and rrSUM149 cells. GAPDH was used as a loading control. (E) Western immunoblot analysis of basal catalase and SOD2 expression in untreated SUM149, rSUM149, and rrSUM149 cells. GAPDH and β-actin were used as loading controls.