Xianfeng Gao1, Xiaoya Wang2, Huaiqiang He3, Yang Cao4,5. 1. Department of Neurosurgery, The First Hospital of Jilin University, Changchun City, Jilin Province, 130031, People's Republic of China. 2. Department of Neurosurgery, Nanchong Central Hospital, The Second Clinical Medical College, North Sichuan Medical College, Nanchong City, Sichuan Province, 637000, People's Republic of China. 3. Department of Intensive Medicine, The First Hospital of Jilin University, Changchun City, Jilin Province, 130031, People's Republic of China. 4. Department of Clinical Laboratory, The First Hospital of Jilin University, Changchun City, Jilin Province, 130031, People's Republic of China. YangCaoChangchun@163.com. 5. Department of Clinical Laboratory, The First Hospital of Jilin University, No. 3302 Jilin Road, Erdao District, Changchun City, Jilin Province, ,130021, People's Republic of China. YangCaoChangchun@163.com.
Abstract
BACKGROUND: Glioma is a common brain malignancy, and the purpose of this study is to investigate the function of LINC02308 in glioma. METHODS: The differentially expressed lncRNAs were screened by microarray. The expression of LINC02308 in glioma tissues and cells was evaluated. The interaction among LINC02308, miR-30e-3p, and TM4SF1 was determined. Cell proliferation and apoptosis were evaluated. The expression of mTOR/AKT-signaling and apoptosis-related markers was detected by Western blot. A xenograft tumor mouse model was constructed to investigate the roles of LINC02308. RESULTS: LINC02308 was significantly overexpressed in glioma, and a high LINC02308 level was correlated with a poor prognosis. LINC02308 silencing markedly inhibited proliferation and reduced apoptosis of glioma cells and also suppressed tumor growth in the xenograft tumor mouse model. Finally, we demonstrated that LINC02308 played its oncogenic role through binding to miR-30e-3p so as to relieve miR-30e-3p-induced suppression of TM4SF1. CONCLUSIONS: LINC02308 promoted glioma tumorigenesis as a sponge of miR-30e-3p to upregulate TM4SF1 and activate AKT/mTOR pathway. Graphical Abstract Hypothesis diagram illustrates the function and mechanism of LINC02308 in glioma. A schematic representation of the functional mechanism of LINC02308 in glioma.
BACKGROUND: Glioma is a common brain malignancy, and the purpose of this study is to investigate the function of LINC02308 in glioma. METHODS: The differentially expressed lncRNAs were screened by microarray. The expression of LINC02308 in glioma tissues and cells was evaluated. The interaction among LINC02308, miR-30e-3p, and TM4SF1 was determined. Cell proliferation and apoptosis were evaluated. The expression of mTOR/AKT-signaling and apoptosis-related markers was detected by Western blot. A xenograft tumor mouse model was constructed to investigate the roles of LINC02308. RESULTS: LINC02308 was significantly overexpressed in glioma, and a high LINC02308 level was correlated with a poor prognosis. LINC02308 silencing markedly inhibited proliferation and reduced apoptosis of glioma cells and also suppressed tumor growth in the xenograft tumor mouse model. Finally, we demonstrated that LINC02308 played its oncogenic role through binding to miR-30e-3p so as to relieve miR-30e-3p-induced suppression of TM4SF1. CONCLUSIONS: LINC02308 promoted glioma tumorigenesis as a sponge of miR-30e-3p to upregulate TM4SF1 and activate AKT/mTOR pathway. Graphical Abstract Hypothesis diagram illustrates the function and mechanism of LINC02308 in glioma. A schematic representation of the functional mechanism of LINC02308 in glioma.
Authors: Prakash Chinnaiyan; Elizabeth Kensicki; Gregory Bloom; Antony Prabhu; Bhaswati Sarcar; Soumen Kahali; Steven Eschrich; Xiaotao Qu; Peter Forsyth; Robert Gillies Journal: Cancer Res Date: 2012-10-01 Impact factor: 12.701
Authors: Xu Chen; Fan Yang; Tianze Zhang; Wei Wang; Wenjin Xi; Yufang Li; Dan Zhang; Yi Huo; Jianning Zhang; Angang Yang; Tao Wang Journal: J Exp Clin Cancer Res Date: 2019-02-22