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Whether IGF-1 LR3's prolonged receptor occupancy exacerbates this suppression more than native IGF-1 has not been studied directly, but the mechanism predicts a greater effect per unit time of receptor engagement [1, 18]

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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