MiR-424-5p Inhibits Proliferation, Invasion and Promotes Apoptosis and Predicts Good Prognosis in Glioma by Directly Tar
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ORIGINAL ARTICLE
MiR-424-5p Inhibits Proliferation, Invasion and Promotes Apoptosis and Predicts Good Prognosis in Glioma by Directly Targeting BFAR Zhe Cheng 1 & Hansheng Shu 1 & Ying Cui 1 & Qiujian Zhang 1 & Biao Zhao 1 & Didi Pan 1 & Qing Chao 1 & Dawei Wang 1 Received: 10 January 2020 / Accepted: 21 May 2020 # Arányi Lajos Foundation 2020
Abstract The biological function of miRNA (miR)-424-5p in glioma has not been clarified. This study was to explore the roles of miR424-5p/Bifunctional apoptosis regulator (BFAR) axis in glioma. Ninety-six pairs of human glioma tissues and their adjacent noncancer tissues were collected. The levels of BFAR and miR-424-5p were detected by quantitative polymerase chain reaction (qPCR) in glioma tissues and cell lines. Moreover, the biological roles of miR-424-5p and BFAR in glioma cells were assessed. We found a miR-424-5p binding site in the 3’UTR of BFAR by using TargetScan 7.2 online database. The miR-424-5p level was dramatically decreased in glioma tissues and cell lines, and the BFAR expression was significantly increased. The BFAR expression was negatively related to the miR-424-5p level in glioma tissues. Compared to patients with high miR-424-5p levels in glioma tissues, patients with low miR-424-5p levels had significantly lower survival rate (χ2 = 13.728 and P < 0.001). Compared to patients with high BFAR levels in glioma tissues, patients with low BFAR levels had significantly higher survival rate (χ2 = 5.516 and P = 0.027). Furthermore, up-regulation of miR-424-5p obviously restrained glioma cells proliferation and invasion, and promoted apoptosis. Besides, knockdown of BFAR also could markedly inhibit the proliferation and invasion, and promote apoptosis. Finally, overexpression of BFAR in glioma cells partially reversed the inhibited effects of miR-424-5p mimic. Knockdown of miR-424-5p restrained glioma cell apoptosis and promoted invasion and proliferation via regulation of BFAR. Keywords Glioma . Bifunctional apoptosis regulator . Prognosis . MicroRNA
Introduction Glioma is one of the most common primary intracranial tumors [1]. Glioma treatment includes surgical resection / radiation therapy / chemotherapy. However, all of these treatment strategies have been shown to be unable to completely inhibit glioma cells, which is an important reason for the extremely high recurrence rate of glioma patients [2]. Studies have shown that the 1-, 2-, and 5-year survival rates of glioma patients are 66.0%, 45.3%, and 24.5% [3]. Zhe Cheng and Hansheng Shu contributed equally to this work. * Qing Chao [email protected] * Dawei Wang [email protected] 1
Department of Neurosurgery, The Second Affiliated Hospital of Bengbu Medical College, No. 220 Hongye Road, West of Longzi Lake, Bengbu, Anhui Province, People’s Republic of China
Previous reports demonstrated that altered microRNA (miR) expression has participated in tumorigenesis [4–8]. Many miRs have been confirmed to be dysregulated in glioma, including miR-93-5p, miR-181, miR-125a, miR-454-3p and 199a-5p [9–13]. Up to no
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