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The most predominant drivers of breast cancer therapeutic resistance are summarized in Figure 4, which include a complex interplay of genetic factors (e.g., PTEN, TP53 mutations, HER2 amplification), epigenetic mechanisms (e.g., DNMT-mediated methylation, EZH2-driven H3K27me3), ncRNAs (e.g., HOTAIR, miR-21 with m6A modifications), apoptosis evasion (e.g., Bcl-2 upregulation), robust DNA repair (e.g., HR, NHEJ), and an immunosuppressive TIME (e.g., T cell exhaustion, MDSC infiltration, PD-L1 overexpression), particularly in TNBC and HER2-positive subtypes, highlighting multifaceted targets for precision oncology
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Cryptopine can reduce the activities of glutathione S-transferase ( GST ) and glutathione reductase ( GR ), depletes intracellular glutathione levels, stimulates lipid peroxidation, and induces cytotoxicity by disrupting the cellular defense system
Pollard, B
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