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. Author manuscript; available in PMC: 2014 Jan 25.
Published in final edited form as: Biochem Biophys Res Commun. 2012 Dec 19;430(4):1277–1282. doi: 10.1016/j.bbrc.2012.11.137

Fig. 1. Proteasome inhibitor MG132 induces NAG-1 expression in glioblastoma cells and causes accumulation of U87MG cells in the sub-G1 phase.

Fig. 1

(A and B) Glioblastoma cells (U87MG, U138MG, T98G, and A172 cells) were treated with 1 μM MG132 for 12 h. (A) NAG-1 mRNA levels were determined by quantitative RT-PCR. Values are mean ± standard deviation (SD) of three independent experiments. * p < 0.05. (B and D) Cell lysates were subjected to Western blotting analysis, and the 35-kDa pro-form of the NAG-1 protein and β-actin are shown. (C and D) Control nontarget siRNA or NAG-1 siRNA were transfected into U87MG cells for 48 h. Cells were then treated with 1 μM MG132 for 24 h. (C) The population of sub-G1 DNA content cells was detected by flow cytometry with propidium iodide staining. Values are mean ± SD of three independent experiments. * p < 0.05.