Nature Medicine
10, 484 - 486 (2004)
Published online: 18 April 2004; | doi:10.1038/nm1042
The translation factor eIF-4E promotes tumor formation and cooperates with c-Myc in lymphomagenesisDavide Ruggero1, 2, 4, Lorenzo Montanaro1, 2, Li Ma1, 2, Wei Xu1, 2, Paola Londei3, Carlos Cordon-Cardo2
& Pier Paolo Pandolfi1, 21
Cancer Biology and Genetics Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA. 2
Department of Pathology, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA. 3
Università di Bari−Dipartimento di Biochimica Medica e Biologica Medica, Piazzale Giulio Cesare 70124 Bari, Italy. 4
Present address: Fox Chase Cancer Center, Human Genetics Program, 333 Cottman Avenue, Philadelphia, Pennsylvania 19111, USA.
Correspondence should be addressed to Pier Paolo Pandolfi p-pandolfi@ski.mskcc.orgThe 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.
MORE ARTICLES LIKE THIS These links to content published by NPG are automatically generated.
|
