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. Author manuscript; available in PMC: 2013 Jan 1.

Published in final edited form as: Cancer Lett. 2011 Sep 24;314(1):102–107. doi: 10.1016/j.canlet.2011.09.020

Fig. 4 — Bortezomib-induced autophagy is dependent on JNK. (A) UMSCC-22A cells were treated with 20 nM bortezomib for 24 or 48 hours in the absence or presence of either JNKi (SP600125, 10 nM) or p38i (SB203580, 10 nM). Following treatment, immunoblotting was performed to detect LC3-II protein or β-actin. (B) UMSCC-22A cells stably expressing GFP-LC3 were treated for 24 hours with 0.1% DMSO, or with bortezomib in the absence or presence of JNKi or p38i. Relocalization of GFP-LC3-II to punctate cytoplasmic dots was visualized as in Figure 1, and the number of puncta/per cell determined. Columns represent the average number of puncta/cell from 3 independent experiments, and error bars the standard error of the means.

Fig. 4 — Bortezomib-induced autophagy is dependent on JNK. (A) UMSCC-22A cells were treated with 20 nM bortezomib for 24 or 48 hours in the absence or presence of either JNKi (SP600125, 10 nM) or p38i (SB203580, 10 nM). Following treatment, immunoblotting was performed to detect LC3-II protein or β-actin. (B) UMSCC-22A cells stably expressing GFP-LC3 were treated for 24 hours with 0.1% DMSO, or with bortezomib in the absence or presence of JNKi or p38i. Relocalization of GFP-LC3-II to punctate cytoplasmic dots was visualized as in Figure 1, and the number of puncta/per cell determined. Columns represent the average number of puncta/cell from 3 independent experiments, and error bars the standard error of the means.