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MiR-153 regulates expression of hypoxia-inducible factor-1α in refractory epilepsy

Guo-Hua Gong _, Feng-Mao An, Yu Wang, Ming Bian, Di Wang and Cheng-Xi Wei

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Oncotarget. 2018; 9:8542-8547. https://doi.org/10.18632/oncotarget.24012

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Guo-Hua Gong1,2,3,*, Feng-Mao An1,2,*, Yu Wang1,2, Ming Bian1,2, Di Wang1,2 and Cheng-Xi 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 contributed equally to this work

Correspondence to:

Cheng-Xi Wei, email: [email protected]

Keywords: epilepsy; mTLE; miR-153; HIF-1α; luciferase reporter assay

Received: September 16, 2017     Accepted: November 13, 2017     Published: January 05, 2018


Mesial temporal lobe epilepsy (mTLE), the most common type of temporal lobe epilepsy (TLE), is particularly relevant due to its high frequency of therapeutic resistance of anti-epileptic therapies. MicroRNAs (miRNAs) have been shown to be dysregulated in epilepsy and neurodegenerative diseases, and we hypothesized that miRNAs could be involved in the pathogenesis of MTLE. The present study aimed to explore the expression and functions of miRNA-153 in mTLE. The expression levels of miRNA-153 in refractory TLE patients were evaluated. The bioinformatics analysis showed that the potential target genes of miR-153 were involved in biological processes, molecular functions, and cellular components. miRNA-153 is significantly dysregulated in temporal cortex and plasma of mTLE patients. We identify HIF-1α as a direct target of miRNA-153, and luciferase reporter assays demonstrated that miR-153 could regulate the HIF-1αexpression via 3'-UTR pairing. These data suggest that miR-153 might represent a useful biomarker and treatment target for patients with mTLE.

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