Silencing of miR-124 induces neuroblastoma SK-N-SH cell differentiation, cell cycle arrest and apoptosis through promoting AHR

• Published in: FEBS letters 2011-11, Vol.585 (22), p.3582-3586
• Main Authors: Huang, Tsui-Chin, Chang, Hsin-Yi, Chen, Cheng-Yu, Wu, Pei-Yi, Lee, Hsinyu, Liao, Yung-Feng, Hsu, Wen-Ming, Huang, Hsuan-Cheng, Juan, Hsueh-Fen
• Format: Article
• Language: English
• Subjects: 3′-untranslated mRNA region; 3′-UTR; AHR; anti-miR-124 miRNA inhibitor; Apoptosis; aryl hydrocarbon receptor; Cell Cycle; Cell Cycle Checkpoints; Cell Differentiation; Gene Silencing; Humans; Inh; inhibitor negative control; MicroRNA; MicroRNAs - genetics; miR-124; miRNA; Mock-Inh; Mock-Pre; Neuroblastoma; Neuroblastoma - genetics; Neuroblastoma - metabolism; Neuroblastoma - pathology; Pre; pre-miR-124 precursor; precursor negative control; Receptors, Aryl Hydrocarbon - genetics; Receptors, Aryl Hydrocarbon - metabolism
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/j.febslet.2011.10.025

► Silencing of miR-124 induces neuroblastoma SK-N-SH cell differentiation, cell cycle arrest and apoptosis. ► miR-124 may suppress the expression of AHR by targeting its 3′-UTR. ► Targeting of miR-124 opens new therapeutic avenues in neuroblastoma. Neuroblastoma is the most common extracranial solid tumor in children. We investigate whether miR-124, the abundant neuronal miRNA, plays a pivotal role in neuroblastoma. Knockdown of miR-124 promotes neuroblastoma SK-N-SH cell differentiation, cell cycle arrest and apoptosis. Further miR-124 is predicted to target aryl hydrocarbon receptor (AHR) which may promote neuroblastoma cell differentiation. We validate that miR-124 may suppress the expression of AHR by targeting its 3′-UTR. These results suggest that miR-124 could serve as a potential therapeutic target of neuroblastoma.