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Systematic identification of a nuclear receptor-enriched predictive signature for erastin-induced ferroptosis. | LitMetric

Systematic identification of a nuclear receptor-enriched predictive signature for erastin-induced ferroptosis.

Redox Biol

College of Pharmacy, Seoul National University, Seoul, 08826, Republic of Korea; Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul, 08826, Republic of Korea. Electronic address:

Published: October 2020

AI Article Synopsis

  • Erastin is a synthetic compound that targets cancer cells with an oncogenic RAS mutation by inducing ferroptosis through inhibition of cystine/glutamate antiporters.
  • Researchers found that a redox imbalance in lung cancer cells depletes glutathione, leading to ferroptosis, and identified transcription factors like NRF2 and AhR as key markers for resistance to erastin.
  • Using an integrated gene expression model based on the nuclear receptor meta-pathway (NRM), the study suggests that this approach could help classify patients better for treatments with erastin across various cancer types.

Article Abstract

Erastin, a synthetic lethal compound against cancer expressing an oncogenic RAS, inhibits cystine/glutamate antiporters and causes ferroptosis. However, despite recent evidence for the mechanisms underlying ferroptosis, molecular biomarkers of erastin-dependent ferroptosis have not been identified. Here, we employed isogenic lung cancer cell models to show that a redox imbalance leads to glutathione depletion and ferroptosis. Subsequent transcriptome analysis of pan-cancer cell lines revealed that the activity of transcription factors, including NRF2 and AhR, serve as important markers of erastin resistance. Based on the integrated expression of genes in the nuclear receptor meta-pathway (NRM), we constructed an NRM model and validated its robustness using an independent pharmacogenomics dataset. The NRM model was further evaluated by sensitivity tests on nine cancer cell lines for which erastin sensitivities had not been determined. Our pharmacogenomics approach has the potential to pave the way for the efficient classification of patients for therapeutic intervention using erastin.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7519368PMC
http://dx.doi.org/10.1016/j.redox.2020.101719DOI Listing

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