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. Author manuscript; available in PMC: 2017 Sep 1.
Published in final edited form as: Matrix Biol. 2016 Mar 22;55:22–34. doi: 10.1016/j.matbio.2016.03.006

Figure 3.

Figure 3

Chemotherapy activates NF-κB to stimulate heparanase expression. (A) Levels of HPSE, total IκB, and GAPDH protein in RPMI-8226 (top panel) and U266 (bottom panel) cell extracts after treatment with increasing concentrations of BTZ or CFZ for 14 h. (B) Myeloma cell lines were pretreated with different inhibitors of IKKβ, BMS-345541 (BMS, 5 μM) or BAY11-7082 (BAY, 4 μM) for 2 h prior to incubation with BTZ (25 nM) for 12 h. At end of the incubation, cell extracts were probed by western blotting for HPSE, total IκB, and GAPDH. (C) CAG HPSE-high cells were pretreated with BMS-345541 (5 μM) or BAY11-7082 (4 μM) for 2 h and then incubated with BTZ for 12 h. After incubation, HPSE was probed by western blotting. Arrow points to pro-HPSE (~65 kDa), arrowhead points to active HPSE (~50 kDa). (D) Western blots for HPSE in extracts of myeloma cells treated with BTZ (25 nM) alone or with increasing concentrations of ROS inhibitor, N-acetyl L-cysteine (LNAC) for 14 h. (E) Western blot for heparanase in extracts from LR5 cells treated for 14 h with BMS-345541 (5 μM) or DMSO.

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