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

Cancer Cell. 2011 Jun 14;19(6):765-75. doi: 10.1016/j.ccr.2011.04.018.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Cell Cycle
  • Cell Transformation, Neoplastic / metabolism*
  • Cytoplasm / metabolism
  • Disease Progression
  • Genes, myc
  • Lymphoma / etiology*
  • Lymphoma / pathology
  • Mice
  • Mice, Inbred C57BL
  • Peptide Initiation Factors / physiology*
  • Protein Biosynthesis
  • Protein Kinase C / physiology
  • Protein Kinase C beta
  • Tumor Suppressor Protein p53 / physiology

Substances

  • Itgb4bp protein, mouse
  • Peptide Initiation Factors
  • Tumor Suppressor Protein p53
  • Protein Kinase C
  • Protein Kinase C beta