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. 2016 Jan 27;7(8):9026–9040. doi: 10.18632/oncotarget.7030

Figure 3. PN does not induce lysosomal, proteasomal and caspase-dependent degradation of MITF-M as shown by immunoblotting.

Figure 3

A. DMBC21 cells were treated with 10 and 20 μM PN for the indicated time and the levels of MITF-M, phosphorylated p65 (p-p65), p65, phosphorylated ERK1/2 (p-ERK1/2) and total ERK1/2 were assessed. B. Basal levels of p-ERK1/2 in DMBC cell populations shown by immunoblotting were quantified relatively to the level in A375 cells (n = 3). C. Cells were exposed to 20 μM PN and 0.5 μM trametinib (TRA) alone or in combination for 4 hours with 2 hours preincubation with either drug and protein levels were determined by Western blotting. D. and E. Cells were preincubated with bortezomib (0.1 μM BOR; 10 min), chloroquine (50 μM CQ; 10 min) or caspase inhibitors (50 μM zDEVD or 50 μM zVAD; 30 min) and 20 μM PN was added for additional 4 hours. MCL-1 was used as a control of BOR-triggered inhibition of proteasomal turnover, PARP as a control of caspase inhibition. Equal loading was confirmed by β-actin or ERK1/2. Representative results are shown.