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EnglishBackground: The T-cell lymphoma cell line HuT78B1, selected for resistance to Fas-mediated apoptosis, resulted unexpectedly resistant to the apoptotic and cytotoxic effects of gemcitabine (dFdC). We investigated whether this resistance was due to the impairment of the Fas/Fas-ligand (FasL) system. Materials and Methods: dFdC effects were studied in HuT78B1 and in the parental Fas-sensitive HuT78 cells exposed to inhibitors of the Fas/FasL system. Results: FasL- and Fas-blocking antibodies did not interfere with dFdC-induced apoptosis in HuT78 cells, whereas inhibitors of caspase-8, -9, -1 or -3 had partial inhibitory effects. Notably, in HuT78B1 cells there was a markedly reduced dFdC accumulation notwithstanding a high activity of the activating enzyme deoxycytidine kinase. dFdC accumulation in HuT78 cells was unaffected by a Fas-blocking antibody. Conclusion: This is the first time that the selection of a Fas-resistant cell line led to the isolation of a cell clone unable to accumulate the deoxycytidine analog dFdC. Our results show that this alteration is independent from the impairment of the Fas/FasL system.
Meli, M., Tolomeo, M., D'Alessandro, N., Grimaudo, S., NOTARBARTOLO DI VILLAROSA, M., Papoff, G., et al. (2004). Resistance to gemcitabine in a lymphoma cell line resistant to Fas-mediated apoptosis. ANTICANCER RESEARCH, 24(2 B), 851-857.
| Data di pubblicazione: | 2004 | |
| Titolo: | Resistance to gemcitabine in a lymphoma cell line resistant to Fas-mediated apoptosis | |
| Autori: | ||
| Citazione: | Meli, M., Tolomeo, M., D'Alessandro, N., Grimaudo, S., NOTARBARTOLO DI VILLAROSA, M., Papoff, G., et al. (2004). Resistance to gemcitabine in a lymphoma cell line resistant to Fas-mediated apoptosis. ANTICANCER RESEARCH, 24(2 B), 851-857. | |
| Rivista: | ||
| Abstract: | Background: The T-cell lymphoma cell line HuT78B1, selected for resistance to Fas-mediated apoptosis, resulted unexpectedly resistant to the apoptotic and cytotoxic effects of gemcitabine (dFdC). We investigated whether this resistance was due to the impairment of the Fas/Fas-ligand (FasL) system. Materials and Methods: dFdC effects were studied in HuT78B1 and in the parental Fas-sensitive HuT78 cells exposed to inhibitors of the Fas/FasL system. Results: FasL- and Fas-blocking antibodies did not interfere with dFdC-induced apoptosis in HuT78 cells, whereas inhibitors of caspase-8, -9, -1 or -3 had partial inhibitory effects. Notably, in HuT78B1 cells there was a markedly reduced dFdC accumulation notwithstanding a high activity of the activating enzyme deoxycytidine kinase. dFdC accumulation in HuT78 cells was unaffected by a Fas-blocking antibody. Conclusion: This is the first time that the selection of a Fas-resistant cell line led to the isolation of a cell clone unable to accumulate the deoxycytidine analog dFdC. Our results show that this alteration is independent from the impairment of the Fas/FasL system. | |
| Appare nelle tipologie: | 1.01 Articolo in rivista |
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