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Int. J. Mol. Sci. 2017, 18(8), 1718; doi:10.3390/ijms18081718

Iron, Oxidative Damage and Ferroptosis in Rhabdomyosarcoma

Department of Molecular and Translational Medicine (DMMT), University of Brescia, Viale Europa 11, 25123 Brescia, Italy
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Received: 28 June 2017 / Revised: 2 August 2017 / Accepted: 3 August 2017 / Published: 7 August 2017
(This article belongs to the Special Issue Metal Metabolism in Animals II)
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Abstract

Recent data have indicated a fundamental role of iron in mediating a non-apoptotic and non-necrotic oxidative form of programmed cell death termed ferroptosis that requires abundant cytosolic free labile iron to promote membrane lipid peroxidation. Different scavenger molecules and detoxifying enzymes, such as glutathione (GSH) and glutathione peroxidase 4 (GPX4), have been shown to overwhelm or exacerbate ferroptosis depending on their expression magnitude. Ferroptosis is emerging as a potential weapon against tumor growth since it has been shown to potentiate cell death in some malignancies. However, this mechanism has been poorly studied in Rhabdomyosarcoma (RMS), a myogenic tumor affecting childhood and adolescence. One of the main drivers of RMS genesis is the Retrovirus Associated DNA Sequences/Extracellular signal Regulated Kinases (RAS/ERK)signaling pathway, the deliberate activation of which correlates with tumor aggressiveness and oxidative stress levels. Since recent studies have indicated that treatment with oxidative inducers can significantly halt RMS tumor progression, in this review we covered different aspects, ranging from iron metabolism in carcinogenesis and tumor growth, to mechanisms of iron-mediated cell death, to highlight the potential role of ferroptosis in counteracting RMS growth. View Full-Text
Keywords: iron; ferroptosis; oxidative damage; rhabdomyosarcoma iron; ferroptosis; oxidative damage; rhabdomyosarcoma
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Fanzani, A.; Poli, M. Iron, Oxidative Damage and Ferroptosis in Rhabdomyosarcoma. Int. J. Mol. Sci. 2017, 18, 1718.

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