Figure S4 from Recharacterization of the Tumor Suppressive Mechanism of RSL3 Identifies the Selenoproteome as a Druggable Pathway in Colorectal Cancer

Key Points

MAIN FINDING: RSL3's tumor suppressive mechanism highlights the selenoproteome as a potential therapeutic target.
KEY EVIDENCE: CETSA data indicates no direct interaction between GPX4 and auranofin in treated colorectal cancer cells.
APPROACH: Supplementary Figure S4 presents experimental data focusing on drug interaction studies.
SIGNIFICANCE: Identifying the selenoproteome as a druggable pathway could lead to new treatments for colorectal cancer.

Supplementary data reveals that GPX4 does not interact with auranofin, suggesting a unique aspect of the selenoproteome in colorectal cancer.

Supplementary Figure S4 provides CETSA data to illustrate the absence of direct GPX4 interaction with the compound auranofin in treated cells.

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DeAngelo et al. (2025) studied this question.

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