Long non-coding RNA TUG1 acts as a miR-26a sponge in human glioma cells

• Published in: Biochemical and biophysical research communications Vol. 477; no. 4; pp. 743 - 748
• Main Authors: Li, Jun, An, Gang, Zhang, Meng, Ma, Qingfang
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 02.09.2016
• Subjects: 3' untranslated regions; Binding Sites; bioinformatics; Brain Neoplasms - genetics; Brain Neoplasms - metabolism; Brain Neoplasms - pathology; gene expression regulation; Gene Expression Regulation, Neoplastic - genetics; genes; Glioma; Glioma - genetics; Glioma - metabolism; Glioma - pathology; Humans; luciferase; MicroRNAs - chemistry; MicroRNAs - metabolism; miR-26a sponge; neoplasms; non-coding RNA; pathogenesis; prediction; Protein Binding; PTEN; PTEN Phosphohydrolase - metabolism; quantitative polymerase chain reaction; RNA, Long Noncoding - chemistry; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; taurine; TUG1; Tumor Cells, Cultured; Western blotting; PTEN; Glioma; TUG1; miR-26a sponge
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2016.06.129

Long non-coding RNA taurine upregulated gene 1 (TUG1) acts as an important regulator in cancer pathogenesis; however, its functional mechanism in glioma development remains unclear. This study aims to explore the potential function of TUG1 in glioma by sponging miR-26a. The expression of TUG1, miR-26a, and phosphatase and tensin homolog (PTEN) in 20 paired glioma tissues was detected by quantitative real-time PCR and subjected to correlation analysis. Bioinformatics analysis was performed by using DIANA Tools. Abnormal TUG1 expression was conducted in two glioma cells to analyze its regulation on miR-26a and PTEN using real-time PCR, western blot, and luciferase reporter assay. TUG1 expression was confirmed to be upregulated in glioma tissues, and showed an inverse correlation with downregulated miR-26a. TUG1 could negatively regulate the expression of miR-26a in glioma cells. The bioinformatics prediction revealed putative miR-26a binding sites within TUG1 transcripts. Further experiments demonstrated the positive regulation of TUG1 on the miR-26a target, PTEN, wherein TUG1 could inhibit the negative regulation of miR-26a on PTEN by binding its 3′UTR. Additionally, the expression of PTEN was also upregulated in glioma tissues, showing a positive or negative correlation with TUG1 or miR-26a, respectively. TUG1 could serve as a miR-26a sponge in human glioma cells, contributing to the upregulation of PTEN. This study revealed a new TUG1/miR-26a/PTEN regulatory mechanism and provided a further understanding of the tumor-suppressive role of TUG1 in glioma development. •TUG1 expression was inversely correlated with miR-26a expression in glioma tissues.•miR-26a expression was negatively regulated by TUG1 in two glioma cells.•Putative miR-26a binding sites were revealed within TUG1 manuscripts.•TUG1 could positively regulate PTEN expression by sponging miR-26a.•PTEN expression also correlated with TUG1 and miR-26a expression in glioma tissues.