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Mechanistically, ROS exert their pro-tumorigenic effects mainly through activation of ERK/MAPK, PI3K/AKT, and STAT3 pathways representing a paradigm shift from viewing ROS solely as cytotoxic molecules to recognizing them as key signaling intermediates in HCC development
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Tissue distribution of carnitine biosynthetic enzymes in man
The predicted interaction footprint extends further toward the intracellular region, yielding a broad contact network that plausibly stabilizes an activation-compatible receptor architecture from the extracellular face toward the cytoplasmic side (Figure 4)
However, the efficacy of these agents remains controversial in conditions such as breast cancer and endometrial cancer (EC), underscoring the importance of elucidating their mechanisms of action in malignancies (12-14)
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