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- W3188186656 abstract "4875 4-hydroxy(phenyl)retinamide (4-HPR or fenretinide) is a retinamide capable of inducing apoptosis in some cancer cells. The effects of 4-HPR have been investigated in ESFT cells lines. Treatment with 4-HPR (0.75–10 μM) decreased viable cell number of all 6 ESFT cell lines studied, in a dose dependent manner. The IC50 for the ESFT cell line TC32 was 0.95μM, compared to 5.3 μM for the neuroblastoma cell line SY5Y. The greater sensitivity of TC-32 cells to 4-HPR-induced death compared to the neuroblastoma SY5Y cells suggests a novel mechanism of action. The decrease in ESFT viable cell number reflects 4-HPR-induced apoptosis, demonstrated by an increase in annexin V and propidium iodide positive cells after 10h, and was analysed by FACs. Furthermore, PARP cleavage, evaluated by western blot was identified after 10h treatment with 4-HPR (1.5μM). The reactive oxygen species (ROS) responsive dye CM-H 2 DCFDA was used to measure ROS levels in TC-32 cells before and after treatment with 4-HPR, fluorescence was analysed by FACs. A 6.5-fold increase in ROS was evident within 1h exposure of TC-32 cells to 4-HPR (1.5 μM). To assess the functional consequence of ROS accumulation TC-32 cells were pre-treated with the anti-oxidant ascorbic acid (100 μM, 1 h). This resulted in the rescue of TC-32 cells from 4-HPR-induced cell death and inhibited the accumulation of ROS. These results suggest that ROS is an essential component of 4-HPR-induced cell death in TC-32 cells, consistent with previous studies in other cancer cell types. Interestingly, pre-treatment of TC-32 cells with the p38-inhibitor SB202190 (6.7 μM, 1h) rescued TC-32 cells from 4-HPR-induced death (1.5μM; 48h), demonstrated by decreased apoptosis and increased viable cell number. Treatment with SB202190 also prevented PARP cleavage induced by 4-HPR (1.5μM, 24h). These data suggest that 4-HPR mediates apoptosis through a ROS-dependent mechanism in TC-32 cells. This may directly or indirectly activate the p38 stress-activated kinase pathway leading to PARP cleavage and induction of ESFT cell death. The activation of p38 may in part be responsible for the increased sensitivity of ESFT cells to 4HPR-induced death compared to neuroblastoma cells." @default.
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- W3188186656 date "2004-04-01" @default.
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- W3188186656 title "4-hydroxy(phenyl)retinamide induced death in cell lines of the Ewing’s sarcoma family of tumours (ESFT)" @default.
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