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Related Experiment Video

Updated: Jun 8, 2026

Protocol for the Differentiation of Human Induced Pluripotent Stem Cells into Mixed Cultures of Neurons and Glia for Neurotoxicity Testing

Protocol for the Differentiation of Human Induced Pluripotent Stem Cells into Mixed Cultures of Neurons and Glia for Neurotoxicity Testing

Published on: June 9, 2017

Ionizing radiation activates the Nrf2 antioxidant response.

J Tyson McDonald¹, Kwanghee Kim, Andrew J Norris

¹Division of Molecular and Cellular Oncology, Department of Radiation Oncology, and Pasarow Mass Spectrometry Laboratory, David Geffen School of Medicine at University of California, Los Angeles, California 90095-1714, USA.

Cancer Research

|October 14, 2010

Summary

The Nrf2-ARE pathway protects cancer cells from radiation damage but activates slowly. Nrf2 deficiency increases sensitivity to radiation therapy, highlighting its role in cellular defense.

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Last Updated: Jun 8, 2026

Protocol for the Differentiation of Human Induced Pluripotent Stem Cells into Mixed Cultures of Neurons and Glia for Neurotoxicity Testing

Protocol for the Differentiation of Human Induced Pluripotent Stem Cells into Mixed Cultures of Neurons and Glia for Neurotoxicity Testing

Published on: June 9, 2017

Area of Science:

Molecular Biology
Cancer Research
Radiation Oncology

Background:

The transcription factor Nrf2 (NF-E2-related factor 2) regulates cellular antioxidant defenses.
Nrf2 overexpression is observed in several cancers, but its role in radiation response is unclear.

Purpose of the Study:

To investigate the role of the Nrf2-ARE pathway in breast cancer cell response to ionizing radiation.
To determine the kinetics and functional significance of Nrf2 activation by radiation.

Main Methods:

Ionizing radiation exposure (2-8 Gy) and fractionated doses on breast cancer cells.
Analysis of ARE-dependent transcription, Nrf2-ARE gene/protein markers (e.g., heme oxygenase-1).
Studies using Nrf2-deficient fibroblasts, reactive oxygen species measurements, and clonogenic survival assays.

Main Results:

Radiation dose-dependently activated ARE-dependent transcription in breast cancer cells, with a five-day delay.
Nrf2-deficient cells showed impaired responses and increased sensitivity to radiation.
Nrf2 deletion elevated basal reactive oxygen species and increased radiation-induced ROS.

Conclusions:

The Nrf2-ARE pathway is a critical, albeit delayed, adaptive response conferring radioresistance.
This pathway's activation by radiation may influence tumor response in clinical settings.
Targeting Nrf2 could be a strategy to enhance radiation therapy efficacy.