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SFN promotes the phosphorylative degradation of -catenin while concurrently suppressing downstream targets including c-Myc and cyclin D1, effectively dismantling the transcriptional program that drives CSC self-renewal ( Complementing this mechanism, SFN demonstrates sophisticated regulation of the Notch pathway through a cascade of molecular events

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In this population, different features, such as oxidative stress, inflammation, energy depletion, and uremic toxins, may exacerbate eryptosis [208, 231, 247]

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