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Fig. 4 | Journal of Experimental & Clinical Cancer Research

Fig. 4

From: In vitro and in vivo cytotoxicity of troglitazone in pancreatic cancer

Fig. 4

Involvement of Akt and MAPK signaling in TGZ-induced cell death. a Akt and MAPK protein expression. Cells (1.75 × 106) were pre-cultured for 24 h in 100-mm dishes and treated with TGZ (50 μM) for various durations. Protein (15 μg) was analyzed by western blot for expression of Akt, ERK, JNK, p38, and the phosphorylated forms of each protein. β-Actin was used as a loading control. b Effects of a JNK inhibitor (SP600125) and a p38 inhibitor (SB202190) on TGZ-induced cell death. Cells were pre-cultured for 24 h at density of 1 × 104 cells/well in 96-well plates and then exposed to TGZ (50 μM) in the presence or absence of SP600125 or SB202190 (1 and 3 μM, respectively) for 24 h. Cell viability was assessed by fluorescence assay and is expressed as mean + SD (n = 3–5). Statistical significance was assessed by Dunnett’s test (TGZ vs. TGZ + inhibitors, n.s., not significant). MAPK, mitogen-activated protein kinase; ERK, extracellular signal-regulated kinase; JNK, c-Jun N-terminal kinase; TGZ, troglitazone

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