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The aim was to identify therapeutic targets to enhance NSCLC treatment effectiveness through USP54's role in ferroptosis.

USP54 Promotes Ferroptosis in Non‐Small Cell Lung Cancer by Mediating FOXA2 Deubiquitination and Enhancing ACSL4 Transcription

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The aim was to identify therapeutic targets to enhance NSCLC treatment effectiveness through USP54's role in ferroptosis.
Examined USP54's role in ferroptosis using MTT assay.
Assessed reactive oxygen species, ferrous iron, and malondialdehyde levels.
Investigated molecular mechanisms with coimmunoprecipitation and dual‐luciferase reporter assays.
USP54 overexpression inhibited NSCLC cell proliferation and induced ferroptosis.
Increased levels of ROS, Fe 2+ , and MDA were observed following USP54 overexpression.
USP54 mediated FOXA2 deubiquitination, enhancing its stability and promoting ACSL4 transcription.

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Experimental analysis reveals USP54 induces ferroptosis in NSCLC, suggesting FOXA2 stabilization may enhance therapeutic targets.

Wei et al. (2025) studied this question.

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