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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. 3 — Bortezomib induces JNK activation and JNK-dependent phosphorylation of Bcl-2. (A) UMSCC-22A and 1483 cells were left untreated, treated for 24 hours with 0.1% DMSO, or were treated with 20 nM bortezomib for 24 or 48 hours. Immunoblotting was performed using antibodies directed against phospho-JNK (arrows indicate the location of phospho-JNK1 and phospho-JNK2), total JNK proteins, phospho-serine 70 Bcl-2, or total Bcl-2. Similar results were obtained in 3 independent experiments. (B) Cells were treated as in (A) in the absence or presence of either 10 nM SP600125 (JNK inhibitor (JNKi)) or 10 nM SB203580 (p38 inhibitor (p38i)). Immunoblotting was performed to detect either phosphorylated (phospho-serine 70) Bcl-2 or total Bcl-2 protein. Densitometry was used to determine p-Bcl-2(phospho-Bcl-2)/β-actin and Bcl-2(total Bcl-2)/β-actin ratios.

Fig. 3 — Bortezomib induces JNK activation and JNK-dependent phosphorylation of Bcl-2. (A) UMSCC-22A and 1483 cells were left untreated, treated for 24 hours with 0.1% DMSO, or were treated with 20 nM bortezomib for 24 or 48 hours. Immunoblotting was performed using antibodies directed against phospho-JNK (arrows indicate the location of phospho-JNK1 and phospho-JNK2), total JNK proteins, phospho-serine 70 Bcl-2, or total Bcl-2. Similar results were obtained in 3 independent experiments. (B) Cells were treated as in (A) in the absence or presence of either 10 nM SP600125 (JNK inhibitor (JNKi)) or 10 nM SB203580 (p38 inhibitor (p38i)). Immunoblotting was performed to detect either phosphorylated (phospho-serine 70) Bcl-2 or total Bcl-2 protein. Densitometry was used to determine p-Bcl-2(phospho-Bcl-2)/β-actin and Bcl-2(total Bcl-2)/β-actin ratios.

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