Research Papers:

This article has been corrected. Correction in: Oncotarget. 2018; 9:24871.

MiR-124 acts as a target for Alzheimer’s disease by regulating BACE1

Fengmao An, Guohua Gong, Yu Wang, Ming Bian, Lijun Yu and Chengxi Wei _

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Oncotarget. 2017; 8:114065-114071. https://doi.org/10.18632/oncotarget.23119

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Fengmao An1,2,*, Guohua Gong1,2,3,*, Yu Wang1,2, Ming Bian1,2, Lijun Yu1,2 and Chengxi Wei1,2

1Medicinal Chemistry and Pharmacology Institute, Inner Mongolia University for The Nationalities, Tongliao, Inner Mongolia, P.R. China

2Inner Mongolia Key Laboratory of Mongolian Medicine Pharmacology for Cardio-Cerebral Vascular System, Tongliao, Inner Mongolia, P.R. China

3First Clinical Medical of Inner Mongolia University for Nationalities, Tongliao, Inner Mongolia, P.R. China

*These authors have contributed equally to this work

Correspondence to:

Chengxi Wei, email: [email protected]

Lijun Yu, email: [email protected]

Keywords: Alzheimer’s disease; miR-124; BACE1; cell viability; cell apoptosis

Received: June 03, 2017     Accepted: November 03, 2017     Published: December 09, 2017


Although large numbers of microRNAs (miRNAs) expressed in Alzheimer disease (AD) have been detected, their functions and mechanisms of regulation remain to be fully clarified. Beta-site Amyloid precursor protein Cleaving Enzyme 1 (BACE1) has been one of the prime therapeutic targets for AD. Here, we identified that miR-124 levels are gradually decreased in AD. In addition, we demonstrated that miR-124 suppresses BACE1 expression by directly targeting the 3′UTR of Bace1 mRNA in vitro. Inhibition of miR-124 significantly increased BACE1 levels in neuronal cells. In contrast, miR-124 overexpression significantly suppressed BACE1 expression in cells. And finally we determined that downregulation of miR-124 alleviated Aβ-induced viability inhibition and decreased apoptosis in SH-SY5Y cells. Our results demonstrated that miR-124 is a potent negative regulator of BACE1 in the cellular AD phenotype and might be involved in the pathogenesis of AD.

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