Schisandrin B inhibits the proliferation and invasion of glioma cells by regulating the HOTAIR–micoRNA-125a–mTOR pathway. Issue 2 (18th January 2017)

• Record Type: Journal Article
• Authors: Jiang, Yan; Zhang, Qiuli; Bao, Jinsuo; Du, Chenghua; Wang, Jian; Tong, Qiang; Liu, Chang
• Is Part Of: NeuroReport. Volume 28:Issue 2(2017)
• Publication Date: 2017-01-18
• Subjects: brain tumor -- lncRNA -- microRNA -- traditional Chinese medicinal -- tumor biology; Neurosciences -- Periodicals; Nervous system -- Periodicals; Neurophysiology -- Periodicals; Nervous System Diseases -- Periodicals; Nervous System Physiological Phenomena -- Periodicals; Neurosciences -- Periodicals; 616.805
• DOI: 10.1097/WNR.0000000000000717
• Languages: English
• ISSNs: 0959-4965

Abstract

Abstract : Glioma is one of the most common malignant central nervous system tumors in humans. Schisandrin B (Sch B) has been confirmed to cause the proliferation and invasion of glioma cells. In the present study, the potential mechanism underlying the antitumor effect of Sch B on glioma cells was investigated. The glioma cell lines, U251 and U87, were exposed to Sch B, and the cell viability, apoptosis, migration, and invasion were determined using the MTT assay, flow cytometry, and transwell assay, respectively. Then, the effects of HOTAIR and miR-125a on tumor biology and the mammalian target of rapamycin (mTOR) protein expression in cell lines exposed to Sch B were investigated. The results showed that Sch B decreased HOTAIR expression and increased miR-125a-5p expression. HOTAIR overexpression decreased miR-125a expression and increased mTOR expression in cells with the treatment of Sch B. The miR-125a inhibitor reversed the effects of HOTAIR downregulation on cell proliferation and migration. On co-incubation with rapamycin, a specific mTOR inhibitor, the cell viability, migration, and invasion were decreased and cell apoptosis was increased in two cell lines exposed to Sch B after the treatment of pcDNA-HOTAIR. In conclusion, Sch B played an inhibitory role in the proliferation and invasion of glioma cells by regulating the HOTAIR–micoRNA-125a–mTOR pathway.