Figure 4From: Inhibition of PI3K/AKT and MAPK/ERK pathways causes activation of FOXO transcription factor, leading to cell cycle arrest and apoptosis in pancreatic cancer Effects of sulforaphane (SFN) on the expression of PTEN, AKT, and MAP kinases; and the effects of PI3K/AKT and MAPK pathways on SFN-induced apoptosis. (A), PANC-1 cells were treated with or without SFN (0-20 μM) for 24 h. The cells were harvested and the expression of PTEN, phospho-AKT, AKT, Ras, phospho-ERK, ERK, phospho-JNK, JNK, phospho-p38 and p38 was measured by Western blotting. (B), PTEN and dominant negative AKT enhance SFN-induced apoptosis. AsPC-1 and PANC-1 cells were transiently transfected with empty vector (pcDNA3.1), PTEN wild type (PTEN-WT) or dominant negative AKT (AKT-DN) along with pCMV-LacZ vector (as transfection control) for 24 h. After medium replacement, cells were treated with SFN (10 μM) for 48 h and, apoptosis was measured by Live Dead Assay. Data represent the mean ± S.D. *, # = significantly different from respective controls, P < 0.05. (C), MEK inhibitor PD98059 enhances SFN-induced apoptosis. AsPC-1 and PANC-1 cells were pretreated with PD98059 (1 μM) followed by treatment with SFN (10 μM) for 48 h and, apoptosis was measured by Live Dead Assay. Data represent the mean ± S.D. *, # = significantly different from respective controls, P < 0.05.Back to article page