Isatin inhibits SH-SY5Y neuroblastoma cell invasion and metastasis through MAO/HIF-1α/CXCR4 signaling

• Published in: Anti-cancer drugs Vol. 28; no. 6; p. 645
• Main Authors: Sun, Wenyan, Zhang, Li, Hou, Lin, Ju, Chuanxia, Zhao, Shengmin, Wei, Yaoyue
• Format: Journal Article
• Language: English
• Published: England 01.07.2017
• Subjects: Cell Line, Tumor; Cell Movement - drug effects; Cell Proliferation - drug effects; Dose-Response Relationship, Drug; Enzyme Activation - drug effects; Extracellular Signal-Regulated MAP Kinases - metabolism; Humans; Hypoxia-Inducible Factor 1, alpha Subunit - antagonists & inhibitors; Hypoxia-Inducible Factor 1, alpha Subunit - biosynthesis; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism; Isatin - pharmacology; Monoamine Oxidase - metabolism; Monoamine Oxidase Inhibitors - pharmacology; Neoplasm Metastasis; Neuroblastoma - drug therapy; Neuroblastoma - metabolism; Neuroblastoma - pathology; Reactive Oxygen Species - metabolism; Receptors, CXCR4 - antagonists & inhibitors; Receptors, CXCR4 - biosynthesis; Receptors, CXCR4 - metabolism; Signal Transduction - drug effects
• ISSN: 1473-5741
• DOI: 10.1097/CAD.0000000000000505

Isatin was reported to possess anticancer activities through its effect on tumor proliferation, apoptosis, and metastasis in vitro and in vivo. This study aimed to elucidate the underlying mechanism behind isatin's ability to inhibit neuroblastoma cell metastasis. Our results demonstrated that isatin could inhibit neuroblastoma cell proliferation, invasion, and migration in a dose-dependent manner. Moreover, isatin inhibited the expression level of monoamine oxidase A as well as that of its downstream protein hypoxia-inducible factor 1α. Further study indicated that isatin inhibited reactive oxygen species production, extracellular signal-regulated kinase activation, vascular endothelial growth factor receptor-1 phosphorylation, and chemokine receptor type 4 expression. All results support the potential antimetastatic effect of isatin in neuroblatoma cells.