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Updated: Aug 23, 2026

Assessment of Selective mRNA Translation in Mammalian Cells by Polysome Profiling
10:00

Assessment of Selective mRNA Translation in Mammalian Cells by Polysome Profiling

Published on: October 28, 2014

Lost in translation: dysregulation of cap-dependent translation and cancer

Mary-Ann Bjornsti1, Peter J Houghton

  • 1Department of Molecular Pharmacology, St. Jude Children's Research Hospital, 332 N. Lauderdale St., Memphis, TN 38105, USA.

Cancer Cell
|June 15, 2004
PubMed

Insights

Dysregulation of cap-dependent translation, driven by the Akt-TOR-eIF4E pathway, confers malignant characteristics and induces cancer by suppressing apoptosis. Targeting this pathway offers potential therapeutic strategies for cancer treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The phosphatidylinositol 3' kinase-Akt pathway is linked to cancer development and apoptosis resistance.
  • Mutations activating the TOR kinase and overexpression of eIF4E are observed in human cancers.
  • Direct causal roles for TOR signaling or eIF4E in cancer genesis have been unclear.

Purpose of the Study:

  • To establish the direct role of dysregulated cap-dependent translation in cancer genesis.
  • To investigate how the Akt-TOR-eIF4E pathway contributes to malignant transformation.
  • To highlight the therapeutic potential of targeting this pathway.

Main Methods:

  • Investigated the link between cap-dependent translation and cancer development.
  • Analyzed the function of the Akt-TOR-eIF4E signaling axis in cancer.
  • Evaluated the impact of dysregulated translation on apoptosis.

Main Results:

  • Dysregulation of cap-dependent translation was shown to confer malignant characteristics.
  • This pathway was found to induce cancer by suppressing apoptosis.
  • Evidence supports a direct role for TOR signaling and eIF4E in cancer genesis.

Conclusions:

  • Aberrant cap-dependent translation is a driver of cancer.
  • The Akt-TOR-eIF4E pathway plays a critical role in tumor formation and survival.
  • Targeting the Akt-TOR-eIF4E pathway presents a promising therapeutic avenue for cancer.

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