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. 2016 May 13;7(25):38078–38090. doi: 10.18632/oncotarget.9348

Figure 5. CiQ derivatives disrupted lysosome function and blocked autophagy in an ERK-dependent manner.

Figure 5

A. CiQ derivative treatment induced phosphorylation of ERK. A549 cells were treated with 2 μM of the indicated CiQ derivative for 8 h, and then subjected to immunoblot with antibodies against the indicated protein. B. U0126 reduced 5e (BO-2222)-induced accumulation of LC3-II and p62. A549 cells were pre-treated with 3 μM U0126 for 14 h and then co-treated with 1 μM 5e for another 8 h. C. U0126 ameliorated CiQ-induced LMP. A549 cells were pre-treated with 3 μM U0126 for 14 h and then co-treated with 0.5 μM of the indicated CiQ derivative for 7 h. The cells were then loaded with LTG, and LTG accumulation was analyzed. D. U0126 reduced 5e-induced LC3 punctae formation. A549 cells were pre-treated with 3 μM U0126 for 14 h and then co-treated with 1 μM 5e for 8 h. LC3 punctae were detected by immunofluorescence staining. At least 300 cells were examined under a fluorescence microscope for each experiment. E. U0126 reduced the cytotoxicity of 5e. A549 cells were treated with the indicated concentration of 5e alone or together with 3 μM U0126 for 72 h. Cell viability was determined using the WST-8 assay. The data represent the mean ± SD of at least three independent experiments. * indicates p < 0.01 as compared to untreated cells and # indicates p < 0.01 as compared to CiQ treatment alone, according to Student's t test.