Sensitization of melanoma cells for TRAIL-induced apoptosis by activation of mitochondrial pathways via Bax.
作者： Sandra-Annika Quast , Anja Berger , Michael Plötz , Jürgen Eberle
DOI: 10.1016/J.EJCB.2013.11.003
关键词: Phosphorylation 、 Antagonist 、 Ligand (biochemistry) 、 Caspase 、 Inhibitor of apoptosis 、 Sensitization 、 Melanoma 、 Cell biology 、 Apoptosis 、 Biology
摘要: The death ligand TRAIL (TNF-related apoptosis-inducing ligand) represents a promising therapeutic strategy for metastatic melanoma, however prevalent and inducible resistance limits its applicability use. Recent work has revealed that combinations with survival pathway inhibitors could efficiently sensitize melanoma cells TRAIL. Here, particular role was attributed to the activation of Bax, which is regulated by phosphorylation. Thus, in explained three major steps, namely high levels antiapoptotic Bcl-2 proteins, inhibitor apoptosis proteins (cIAPs) suppressed Bax activity. Importantly, Bid activated response alone also resistant antagonize Bcl-2, inhibitors. However, only combinations, mitochondrial pathways were opened result release Smac/DIABLO, functions as antagonist cIAPs. Opening caspase cascade Smac then allowed efficient induction apoptosis. direct or indirect targeting suitable overcome may allow establishment TRAIL-based approaches.
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