Title : The molecular mechanism of sensitization to Fas-mediated apoptosis by 2-methoxyestradiol in PC3 prostate cancer cells.

Pub. Date : 2004 Jan

PMID : 14694442






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1 Moreover, we found that inhibition of 2-ME-induced extracellular signal-regulated kinase (ERK) activation by the upstream kinase inhibitor PD98059 significantly enhanced 2-ME-mediated suppression of Akt activation, resulting in much greater sensitization to apoptosis. 2-Methoxyestradiol mitogen-activated protein kinase 1 Homo sapiens
2 Moreover, we found that inhibition of 2-ME-induced extracellular signal-regulated kinase (ERK) activation by the upstream kinase inhibitor PD98059 significantly enhanced 2-ME-mediated suppression of Akt activation, resulting in much greater sensitization to apoptosis. 2-Methoxyestradiol mitogen-activated protein kinase 1 Homo sapiens
3 Moreover, we found that inhibition of 2-ME-induced extracellular signal-regulated kinase (ERK) activation by the upstream kinase inhibitor PD98059 significantly enhanced 2-ME-mediated suppression of Akt activation, resulting in much greater sensitization to apoptosis. 2-Methoxyestradiol mitogen-activated protein kinase 1 Homo sapiens
4 Moreover, we found that inhibition of 2-ME-induced extracellular signal-regulated kinase (ERK) activation by the upstream kinase inhibitor PD98059 significantly enhanced 2-ME-mediated suppression of Akt activation, resulting in much greater sensitization to apoptosis. 2-Methoxyestradiol mitogen-activated protein kinase 1 Homo sapiens
5 Taken together, the present findings indicate that 2-ME suppresses NF-kappaB/FLIP signaling and enhances DISC formation through inhibition of Akt, and that PC3 cells thereby are being sensitized to Fas-mediated apoptosis and by a process closely associated with ERK. 2-Methoxyestradiol mitogen-activated protein kinase 1 Homo sapiens