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They include CAMP-response element binding protein (CREB), SP1 transcription factor (SP1), transcription factor AP-2 (AP2), proliferator-activated receptor alpha (PPAR), all activating GPX4 expression, while Krppel-like transcription factor 2 (KLF2) and CAMP-response element modulator (CREM), both repress its protein expression [7]

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Chen and colleagues have performed some experiments to identify a novel mechanism through which Eriocalyxin B, a natural diterpenoid, induces ferroptosis by suppressing STAT3/SIRT3 transcription and modulating fatty acid metabolism through the SIRT3-SREBP1-PPAR pathway in TNBC, suggesting a novel inducer of ferroptosis for TNBC treatment [150]