The translation factor eIF-4E promotes tumor formation and cooperates with c-Myc in lymphomagenesis
Nature medicine, 2004•nature.com
The mammalian target of rapamycin, mTOR, regulates cell growth and proliferation. Here we
show that the initiation factor of translation (eIF-4E), a downstream effector of mTOR, has
oncogenic effects in vivo and cooperates with c-Myc in B-cell lymphomagenesis. We found
that c-Myc overrides eIF-4E-induced cellular senescence, whereas eIF-4E antagonizes c-
Myc-dependent apoptosis in vivo. Our results implicate activation of eIF-4E as a key event in
oncogenic transformation by phosphoinositide-3 kinase and Akt.
show that the initiation factor of translation (eIF-4E), a downstream effector of mTOR, has
oncogenic effects in vivo and cooperates with c-Myc in B-cell lymphomagenesis. We found
that c-Myc overrides eIF-4E-induced cellular senescence, whereas eIF-4E antagonizes c-
Myc-dependent apoptosis in vivo. Our results implicate activation of eIF-4E as a key event in
oncogenic transformation by phosphoinositide-3 kinase and Akt.
Abstract
The mammalian target of rapamycin, mTOR, regulates cell growth and proliferation. Here we show that the initiation factor of translation (eIF-4E), a downstream effector of mTOR, has oncogenic effects in vivo and cooperates with c-Myc in B-cell lymphomagenesis. We found that c-Myc overrides eIF-4E-induced cellular senescence, whereas eIF-4E antagonizes c-Myc-dependent apoptosis in vivo. Our results implicate activation of eIF-4E as a key event in oncogenic transformation by phosphoinositide-3 kinase and Akt.
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