Long noncoding RNA LINC00511 induced by SP1 accelerates the glioma progression through targeting miR‐124‐3p/CCND2 axis. Issue 6 (11th April 2019)

• Record Type: Journal Article
• Authors: Li, Chen; Liu, Hongjiang; Yang, Jipeng; Yang, Jiankai; Yang, Liang; Wang, Yuanyu; Yan, Zhongjie; Sun, Yuchen; Sun, Xiaofeng; Jiao, Baohua
• Is Part Of: Journal of cellular and molecular medicine. Volume 23:Issue 6(2019)
• Page Start: 4386
• Page End: 4394
• Publication Date: 2019-04-11
• Subjects: CCND2 -- glioma -- LINC00511 -- miR‐124‐3p -- SP1; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.14331
• Languages: English
• ISSNs: 1582-1838

Abstract

Abstract: Mounting evidence suggests the vital roles of long noncoding RNA (lncRNAs) in the glioma. However, the role of LINC00511 in gliomagenesis is still uncovered. Here, in this study, we aim to investigate the effects of LINC00511 on the glioma cancer phenotype and its deepgoing mechanism. Results indicated that LINC00511 was up‐regulated in glioma tissues and cell lines, moreover its overexpression positively correlated with the poor prognosis and advanced pathological stages. For the upstream regulation, LINC00511 was epigenetically up‐regulated by transcription factor specificity protein 1 (SP1). Gain and loss of functional experiments demonstrated that LINC00511 promoted the proliferation and invasion of glioma cells in vitro. The knockdown of LINC00511 repressed the tumour growth in vivo. Mechanistically, LINC00511 positively regulated the CCND2 expression via competitively sponging with miR‐124‐3p. Overall, our finding illuminates that LINC00511 is induced by SP1 and accelerates the glioma progression through targeting miR‐124‐3p/CCND2 axis, constructing the SP1/LINC00511/miR‐124‐3p/CCND2 axis.