细胞毒性菲咯啉衍生物改变神经母细胞瘤细胞中的金属稳态和氧化还原稳态。
Cytotoxic phenanthroline derivatives alter metallostasis and redox homeostasis in neuroblastoma cells.
作者信息
Naletova Irina, Satriano Cristina, Curci Alessandra, Margiotta Nicola, Natile Giovanni, Arena Giuseppe, La Mendola Diego, Nicoletti Vincenzo Giuseppe, Rizzarelli Enrico
机构信息
Department of Chemical Sciences, University of Catania, Catania, Italy.
Consorzio Interuniversitario di Ricerca in Chimica dei Metalli nei Sistemi Biologici (CIRCMSB), Bari, Italy.
出版信息
Oncotarget. 2018 Nov 20;9(91):36289-36316. doi: 10.18632/oncotarget.26346.
Copper homeostasis is generally investigated focusing on a single component of the metallostasis network. Here we address several of the factors controlling the metallostasis for neuroblastoma cells (SH-SY5Y) upon treatment with 2,9-dimethyl-1,10-phenanthroline-5,6-dione (phendione) and 2,9-dimethyl-1,10-phenanthroline (cuproindione). These compounds bind and transport copper inside cells, exert their cytotoxic activity through the induction of oxidative stress, causing apoptosis and alteration of the cellular redox and copper homeostasis network. The intracellular pathway ensured by copper transporters (Ctr1, ATP7A), chaperones (CCS, ATOX, COX 17, Sco1, Sco2), small molecules (GSH) and transcription factors (p53) is scrutinised.
铜稳态通常是围绕金属稳态网络的单个组成部分进行研究的。在此，我们探讨了在用2,9-二甲基-1,10-菲咯啉-5,6-二酮（菲醌）和2,9-二甲基-1,10-菲咯啉（铜菲咯啉）处理后，控制神经母细胞瘤细胞（SH-SY5Y）金属稳态的几个因素。这些化合物在细胞内结合并转运铜，通过诱导氧化应激发挥其细胞毒性活性，导致细胞凋亡以及细胞氧化还原和铜稳态网络的改变。我们仔细研究了由铜转运蛋白（Ctr1、ATP7A）、伴侣蛋白（CCS、ATOX、COX 17、Sco1、Sco2）、小分子（谷胱甘肽）和转录因子（p53）所确保的细胞内途径。
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