Cellular, Molecular and Developmental NeuroscienceLncRNA SNHG4 regulates miR-138/c-Met axis to promote the proliferation of glioblastoma cellsWang, Xiaojiaoa; Tian, Weia; Wu, Liangb; Wei, Zhenqingc; Li, Weihuac; Xu, Yousongc; Li, YangcAuthor Information aDepartment of Nursing, The First Affiliated Hospital of Dalian Medical University, Dalian City, Liaoning Province bDepartment of Neurosurgery, The People’s Hospital of Naqu, Naqu City, Xizang cDepartment of Neurosurgery, The First Affiliated Hospital of Dalian Medical University, Dalian City, Liaoning Province, PR. China Received 12 November 2019 Accepted 28 January 2020 Correspondence to Yang Li, MD, Department of Neurosurgery, The First Affiliated Hospital of Dalian Medical University, No. 222 Zhongshan Road, Dalian City, Liaoning Province 116011, PR. China, Tel: +86 13596849483; fax: +86 13596849483; e-mail: email@example.com NeuroReport: June 10, 2020 - Volume 31 - Issue 9 - p 657-662 doi: 10.1097/WNR.0000000000001469 Buy Metrics Abstract LncRNA SNHG4 has been reported to be an oncogenic lncRNA in osteosarcoma. Our preliminary analysis of the cancer genome atlas dataset revealed the upregulation of SNHG4 in glioblastoma (GBM). In this study, we confirmed the upregulation of SNHG4 in GBM tissues collected from GBM patients. In addition, lower survival rate of GBM patients was observed in patients with high SNHG4 expression level. SNHG4 can directly interact with miR-138, while SNHG4 expression was no altered after miR-138 overexpression. Interestingly, SNHG4 overexpression led to the upregulation of c-Met, a target of miR-138. Cell counting kit-8 assay showed that miR-138 overexpression resulted in decreased proliferation rate of GBM cells. SNHG4 and c-Met overexpression played opposite roles and reduced the effects of miR-138. Therefore, SNHG4 regulates miR-138/c-Met axis to promote the proliferation of GBM cells. Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.