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Related Experiment Video

Updated: Mar 12, 2026

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells

Published on: May 1, 2020

The Bad, the Good and eIF3e/INT6.

Julie Sesen¹, Joshua Casaos², Sarah J Scotland²

¹INSERM U1037, Centre de Recherche en Cancerologie de Toulouse, 2 Avenue Hubert Curien, Toulouse 31100, France.

Frontiers in Bioscience (Landmark Edition)

|November 5, 2016

Summary

This summary is machine-generated.

The translation factor INT6/eIF3e plays a dual role in cancer and ischemic injuries. Understanding its mechanisms could lead to new therapies for vascular diseases and cancer.

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Area of Science:

Molecular Biology
Cell Biology
Biochemistry

Background:

Translational factors are crucial in pathologies like cancer and wound healing.
eIF3e, also known as INT6, is a key translation initiation factor.
INT6/eIF3e has diverse roles including translation, DNA repair, and hypoxia response.

Purpose of the Study:

To review the multifaceted roles of INT6/eIF3e in various pathophysiological processes.
To highlight the dual oncogenic and tumor-suppressive functions of INT6/eIF3e.
To explore the therapeutic potential of INT6/eIF3e modulation in diseases like cancer and ischemic injuries.

Main Methods:

Literature review of recent research on INT6/eIF3e.
Analysis of studies investigating INT6/eIF3e's involvement in translation, protein degradation, DNA repair, and hypoxia.
Examination of in vitro and in vivo findings related to INT6/eIF3e's functions.

Main Results:

INT6/eIF3e acts as a "double-edged sword" with both oncogenic and tumor-suppressive properties.
INT6/eIF3e modulates Hypoxia Inducible Factors (HIFs), influencing cellular response to low oxygen.
Silencing INT6/eIF3e shows potential for improving cell survival after ischemic injuries.

Conclusions:

INT6/eIF3e is a critical regulator in tumorigenesis and angiogenic processes.
Further understanding of INT6/eIF3e's molecular mechanisms is essential for clinical applications.
Modulating INT6/eIF3e offers therapeutic promise for cancer and vascular diseases.