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Impairment of cytoplasmic eIF6 activity restricts lymphomagenesis and tumor progression without affecting normal growth.

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.

journal_name

Cancer Cell

journal_title

Cancer cell

authors

Miluzio A,Beugnet A,Grosso S,Brina D,Mancino M,Campaner S,Amati B,de Marco A,Biffo S

doi

10.1016/j.ccr.2011.04.018

subject

Has Abstract

pub_date

2011-06-14 00:00:00

pages

765-75

issue

6

eissn

1535-6108

issn

1878-3686

pii

S1535-6108(11)00163-2

journal_volume

19

pub_type

杂志文章

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