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. 2017 Nov 14;8(64):108006–108019. doi: 10.18632/oncotarget.22444

Figure 6. The effects of CD on activation of AKT and MAPKs in NPC-BM and NPC-039 cells.

Figure 6

(A) Cells were treated with increasing concentrations of CD (0-8 μM) for 24 h. Total cell lysates were analyzed by Western blot with specific antibodies against p-AKT, AKT, p-ERK1/2, ERK1/2, p-p38, p38, p-JNK1/2, p-JNK1/2, and β-actin. (B) The intensity of the phosphorylation signals normalized against their total protein levels. The histogram illustrates the relative phosphorylation levels. (C-J) Effects of the inhibition of AKT, ERK1/2, p38, and JNK1/2 on CD-induced apoptosis and autophagy were assessed by Western blot using specific antibodies (cleaved PARP and LC3-I/LC3-II). Cells were pretreated with LY294002 (AKT inhibitor, 20 μM), U0126 (ERK1/2 inhibitor, 10 μM), SB203580 (p38 MAPK inhibitor, 10 μM), or SP600125 (JNK inhibitor, 20 μM) for 1 h followed by treatment with or without CD for 24 h. The intensity of the band signals was quantified by densitometry and normalized to β-actin. The relative expression levels are shown in the histogram (right panel). Values represent the mean ± SEM. from three determinations. *P < 0.05, compared with the control (0 μM). #P < 0.05, compared cells treated with CD (8 μM) alone.