Circular RNA Circ_ANKMY2 Regulates Temporal Lobe Epilepsy Progression via the miR-106b-5p/FOXP1 Axis
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Circular RNA Circ_ANKMY2 Regulates Temporal Lobe Epilepsy Progression via the miR-106b-5p/FOXP1 Axis Qing Lin1 · Jinying Chen1 · Xian Zheng1 · Yi Zhang1 · Xiaoxiao Tao1 · Jiamei Ye1 Received: 6 March 2020 / Revised: 15 September 2020 / Accepted: 14 October 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Temporal lobe epilepsy (TLE) is common intractable epilepsy that affects the patient’s lives. The circular RNA circ_ ANKMY2 (circ_ANKMY2) has been reported to be abnormally expressed in TLE. Nevertheless, the role and mechanism of circ_ANKMY2 in TLE are unclear. A human neuroblastoma cell line (SK-N-AS) was used for a series of studies. Expression levels of circ_ANKMY2, miR-106b-5p, and Forkhead Box Protein 1 (FOXP1) mRNA in TLE tissues were assessed through quantitative real-time polymerase chain reaction (qRT-PCR). Cell colony formation, proliferation, and apoptosis were determined by cell colony formation, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), or flow cytometry assays. The levels of FOXP1 protein, Ki67, B cell lymphoma (Bcl-2), Bcl-2 Associated X (Bax), and Cleaved caspase-3 were evaluated by western blot analysis. The relationship between circ_ANKMY2 or FOXP1 and miR-106b-5p was verified with dual-luciferase reporter assay. We observed that circ_ANKMY2 and FOXP1 expression were reduced while miR-106b-5p expression was increased in TLE tissues. Overexpression of circ_ANKMY2 decreased spontaneous recurrent seizures (SRSs) in rat TLE model and blocked cell colony formation, proliferation, and induced cell apoptosis in SK-N-AS cells. Importantly, circ_ANKMY2 was verified as a sponge for miR-106b-5p. In addition, miR-106b-5p mimics abolished circ_ANKMY2 elevation-mediated effects on colony formation, proliferation, and apoptosis of SK-N-AS cells. Also, FOXP1 served as a target for miR-106b-5p. And FOXP1 silencing overturned the effects of miR-106b-5p inhibitors on the colony formation, proliferation, and apoptosis of SK-N-AS cells. In sum, circ_ANKMY2 modulated TLE advancement via regulation of FOXP1 expression through sponging miR-106b-5p, and circ_ANKMY2 might be an underlying target for the improvement of TLE. Keywords TLE · circ_ANKMY2 · miR-106b-5p · FOXP1
Introduction Temporal lobe epilepsy (TLE) is the most common intractable epilepsy in adults, and it is characterized by periodic and unpredictable seizures [1]. TLE has been thought to be caused by neuronal dysfunction [2]. At present, although many antiepileptic drugs have been developed, there is no Electronic supplementary material The online version of this article (doi:https://doi.org/10.1007/s11064-020-03151-7) contains supplementary material, which is available to authorized users. * Jiamei Ye [email protected] 1
Department of Neurology, The First People’s Hospital of Taizhou, No.218 Hengjie Road, Huangyan District, Taizhou 318020, Zhejiang, China
substantial improvement in the management of TLE [3, 4]. Therefore, it is very important to explore the molecular mech
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