| First Author | Miluzio A | Year | 2011 |
| Journal | Cancer Cell | Volume | 19 |
| Issue | 6 | Pages | 765-75 |
| PubMed ID | 21665150 | Mgi Jnum | J:173559 |
| Mgi Id | MGI:5014451 | Doi | 10.1016/j.ccr.2011.04.018 |
| Citation | Miluzio A, et al. (2011) Impairment of Cytoplasmic eIF6 Activity Restricts Lymphomagenesis and Tumor Progression without Affecting Normal Growth. Cancer Cell 19(6):765-75 |
| abstractText | Eukaryotic Initiation Factor 6 (eIF6) controls translation by regulating 80S subunit formation. eIF6 is overexpressed in tumors. Here, we demonstrate that eIF6 inactivation delays tumorigenesis and reduces tumor growth in vivo. eIF6(+/-) mice resist to Myc-induced lymphomagenesis and have prolonged tumor-free survival and reduced tumor growth. eIF6(+/-) mice are also protected by p53 loss. Myc-driven lymphomas contain PKCbetaII and phosphorylated eIF6; eIF6 is phosphorylated by tumor-derived PKCbetaII, but not by the eIF4F activator mTORC1. Mutation of PKCbetaII phosphosite of eIF6 reduces tumor growth. Thus, eIF6 is a rate-limiting controller of initiation of translation, able to affect tumorigenesis and tumor growth. Modulation of eIF6 activity, independent from eIF4F complex, may lead to a therapeutical avenue in tumor therapy. |
