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Related Experiment Video

Updated: Sep 7, 2025

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

Inhibition of the Translation Initiation Factor eIF4A Enhances Tumor Cell Radiosensitivity.

Stacey L Lehman¹, Theresa Wechsler¹, Kayla Schwartz¹

¹Radation Oncology Branch, NCI, Bethesda, Maryland.

Molecular Cancer Therapeutics

|June 22, 2022

Summary

Targeting eukaryotic translation initiation factor 4A (eIF4A) with inhibitors can enhance tumor radiosensitivity. This approach selectively sensitizes cancer cells to radiation by inhibiting DNA repair, showing promise for cancer treatment.

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Area of Science:

Molecular Biology
Cancer Research
Radiotherapy

Background:

Translational control of gene expression is crucial for cellular radioresponse.
The eukaryotic translation initiation factor 4F (eIF4F) cap binding complex regulates translation.
eIF4A, an RNA helicase component of eIF4F, is investigated as a potential radiosensitization target.

Purpose of the Study:

To investigate whether the RNA helicase eIF4A can serve as a target for radiosensitization.
To evaluate the effects of eIF4A inhibition on tumor cell radiosensitivity and DNA repair.
To assess the in vivo efficacy of an eIF4A inhibitor, (-)-SDS-1021, in combination with radiation.

Main Methods:

Knockdown of eIF4A using siRNA to assess translational efficiency and radiosensitivity.
Treatment of tumor cells and normal fibroblasts with the eIF4A inhibitor (-)-SDS-1021.
Analysis of polysome profiles, clonogenic survival, and radiation-induced γH2AX foci dispersal.
In vivo studies using subcutaneous xenografts in mice treated with (-)-SDS-1021 and radiation.

Main Results:

eIF4A knockdown reduced translational efficiency and enhanced tumor cell radiosensitivity, accompanied by delayed DNA repair.
(-)-SDS-1021 treatment decreased translational efficiency and protein synthesis, enhancing tumor cell radiosensitivity.
This radiosensitization was linked to inhibited DNA double-strand break repair, with no effect on normal cells.
In vivo, (-)-SDS-1021 decreased tumor translational efficiency and significantly enhanced radiation-induced tumor growth delay.

Conclusions:

eIF4A is a tumor-selective target for radiosensitization.
Inhibition of eIF4A enhances tumor radiosensitivity by impairing DNA double-strand break repair.
The rocaglate (-)-SDS-1021 demonstrates potential as a therapeutic agent to improve radiotherapy outcomes.