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Translation initiation factor 4E blocks endoplasmic reticulum-mediated apoptosis.

Shunan Li¹, David M Perlman, Mark S Peterson

¹Department of Medicine, University of Minnesota Medical School, Minneapolis, MN 55455, USA.

The Journal of Biological Chemistry

|March 3, 2004

Summary

Eukaryotic translation initiation factor 4E (eIF4E) prevents programmed cell death by regulating endoplasmic reticulum stress responses. This protein impacts cell survival and offers potential therapeutic targets for cancer.

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Area of Science:

Molecular Biology
Cell Biology
Biochemistry

Background:

Eukaryotic translation initiation factor 4E (eIF4E) is crucial for cap-dependent mRNA translation and ribosome recruitment.
Overexpression of eIF4E promotes cell growth, survival, and drug resistance, contributing to malignant transformation.
Previous studies linked eIF4E to the suppression of apoptosis via mitochondrial pathways.

Purpose of the Study:

To investigate the role of ectopic eIF4E expression in apoptosis mediated by the endoplasmic reticulum (ER).

Main Methods:

Cells with ectopic eIF4E expression were exposed to various ER stressors.
Apoptosis induction was assessed in response to stressors like brefeldin A, tunicamycin, thapsigargin, and A23187.
Calcium release from the ER and caspase-12 translocation were monitored.

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Main Results:

Ectopic eIF4E expression conferred resistance to ER stressors, preventing apoptosis.
Cells rescued from Ca(2+) ionophore-induced apoptosis showed no significant calcium release from the ER.
Caspase-12 did not translocate from the ER to the cytoplasm in eIF4E-rescued cells.

Conclusions:

eIF4E acts as a pleiotropic regulator of cell viability, influencing apoptosis.
The cap-dependent translation machinery can control organelle-mediated apoptotic checkpoints.
eIF4E's role in ER stress response highlights its significance in cell survival and cancer biology.