AI Article Synopsis
- Eukaryotic Initiation Factor 6 (eIF6) is key in regulating protein translation and is found to be overexpressed in tumors.* -
- Research shows that mice with reduced eIF6 levels (eIF6(+/-)) have slower tumor development, especially in Myc-induced lymphomas, and enjoy extended periods without tumors.* -
- eIF6's activity, specifically its phosphorylation by PKCβII, plays a crucial role in tumor growth, suggesting that targeting eIF6 could provide new treatment options for cancer.*
Article Abstract
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 PKCβII and phosphorylated eIF6; eIF6 is phosphorylated by tumor-derived PKCβII, but not by the eIF4F activator mTORC1. Mutation of PKCβII 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.
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| http://dx.doi.org/10.1016/j.ccr.2011.04.018 | DOI Listing |
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