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. 2015 Nov 27;7(2):1598–1607. doi: 10.18632/oncotarget.6408

Figure 3. Blocking ERK overcomes heparanase-induced chemoresistance of myeloma cells.

Figure 3

(A) Western blots of ubiquitinated protein in cell extracts from HPSE-high and HPSE-low after overnight incubation with BTZ (10 nM). Actin served as the loading control. (B) Viability of HPSE-high cells treated with ERK inhibitors U0126 (25 μM) or PD98059 (PD, 50 μM) for 2 h prior to incubation with BTZ (5 nM), CFZ (7.5 nM) or Mel (10 μM) for 14 h. PD98059 at a concentration of 50 uM is shown to block ERK mediated signaling in our previous studies involving HPSE-high cells [14]. Controls included cells treated with ERK inhibitors or chemotherapeutic drugs alone. Viability was determined by MTT assay, *p < 0.05 versus individual drug treatment alone. (C) Viability of HPSE-high cells treated with either BTZ (5 nM) or MEK inhibitor- AZD6244 (AZ) (200 nM) alone or a combination of the two drugs for 14 h, *p < 0.005 versus BTZ treatment alone. Data are represented as mean ± SEM.