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RSL3 suppresses spheroid formation and viability, and halts migration of PTC cells in vitro We postulated that the RSL3-mediated suppression of thyroid tumor cell viability is a ferroptosis pathway-dependent process, therefore, we treated K1 cells with a lethal dose of RSL3 alone and in the presence of either a ferroptosis inhibitor Fer1, or a pan caspase inhibitor, Z-VAD-FMK (ZVAD) and measured cell viability

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Upregulation of GGT activity is primarily dependent on the Ras protein and its downstream effectors, which include extracellular signal-regulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K)/AKT and c-Jun N-terminal kinase (JNK) signaling pathways (Fig