Fig. 4From: In vitro and in vivo cytotoxicity of troglitazone in pancreatic cancerInvolvement of Akt and MAPK signaling in TGZ-induced cell death. a Akt and MAPK protein expression. Cells (1.75āĆā106) were pre-cultured for 24Ā h in 100-mm dishes and treated with TGZ (50Ā Ī¼M) for various durations. Protein (15Ā Ī¼g) was analyzed by western blot for expression of Akt, ERK, JNK, p38, and the phosphorylated forms of each protein. Ī²-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 24Ā h at density of 1āĆā104 cells/well in 96-well plates and then exposed to TGZ (50Ā Ī¼M) in the presence or absence of SP600125 or SB202190 (1 and 3Ā Ī¼M, respectively) for 24Ā h. Cell viability was assessed by fluorescence assay and is expressed as meanā+āSD (nā=ā3ā5). Statistical significance was assessed by Dunnettās test (TGZ vs. TGZā+āinhibitors, n.s., not significant). MAPK, mitogen-activated protein kinase; ERK, extracellular signal-regulated kinase; JNK, c-Jun N-terminal kinase; TGZ, troglitazoneBack to article page