CIL56 acts by inducing non-apoptotic cell death, triggering cell death dependent upon the rate-limiting de novo lipid synthetic enzyme ACC1.
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Ferroptosis is a non-apoptotic and iron-dependent form of regulated cell death. Ferroptosis is characterized by extensive lipid peroxidation, which can be suppressed by iron chelators or lipophilic antioxidants. CIL56 acts as a potent ferroptosis inducer with novel scaffold. CIL56 showed some degree of selectivity towards oncogenic-RAS-expressing cells in the BJ series. CIL56 induced iron-dependent ROS (reactive oxygen species). CIL56 was capable of engaging two independent death pathways: ferroptosis at low concentrations, and a necrotic, non-suppressible phenotype at higher concentrations. Antioxidants and iron chelators only suppressed the lethality of low concentrations of CIL56[1]. Two clonal ACACA (acetyl-CoA carboxylase alpha; encoding ACC1) null HT-1080 cells lines lacked ACC1 expression and exhibited 5-fold resistance to CIL56. Furthermore, the lethality of CIL56 was suppressed by the small molecule ACC1 inhibitor. These results suggest that CIL56 triggers cell death dependent upon the rate-limiting de novo lipid synthetic enzyme ACC1[2].
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