Abstract
Accumulating evidence has highlighted the potential role of long non-coding RNAs (lncRNAs) as biomarkers and therapeutic targets in solid tumors. Here, we elucidated the function and possible molecular mechanisms of lncRNA KCNQ1OT1 in human glioma U87 and U251 cells. Quantitative Real-Time polymerase chain reaction (qRT-PCR) demonstrated that KCNQ1OT1 expression was up-regulated in glioma tissues and cells. Knockdown of KCNQ1OT1 exerted tumor-suppressive function in glioma cells. Moreover, a binding region was confirmed between KCNQ1OT1 and miR-370 by dual-luciferase assays. qRT-PCR showed that miR-370 was down-regulated in human glioma tissue and cells. In addition, restoration of miR-370 exerted tumor-suppressive function via inhibiting cell proliferation, migration and invasion, while promoting the apoptosis of human glioma cells. Knockdown of KCNQ1OT1 decreased the expression level of Cyclin E2 (CCNE2) by binding to miR-370. Further, miR-370 bound to CCNE2 3′UTR region and decreased the expression of CCNE2. These results provided a comprehensive analysis of KCNQ1OT1-miR-370-CCNE2 axis in human glioma cells and might provide a novel strategy for glioma treatment.
Highlights
Gliomas are one of the most life-threatening and common primary human brain malignancies with an annual incidence of five cases per 100,000 people
Knockdown of KCNQ1OT1 suppressed the malignant behaviors of human glioma U87 and U251 cells
The KCNQ1OT1 knockdown up-regulated miR-370, which was lowly expressed in glioma tissues and cells
Summary
Gliomas are one of the most life-threatening and common primary human brain malignancies with an annual incidence of five cases per 100,000 people. Long non-coding RNAs (lncRNAs) have been confirmed to act as key molecules in cancer development and progression (Cloutier et al, 2016; Liu et al, 2016). Dysregulations of lncRNAs are discovered in various tumor tissues and cancer cells where they serve as oncogenes or tumor suppressors (Ellinger et al, 2015; Jiang et al, 2016). KCNQ1OT1, an imprinted antisense lncRNA in the human KCNQ1 locus on chromosome 11p15.5, is involved in cis-limited silencing within an imprinted KCNQ1 cluster (Zhang et al, 2014; Sunamura et al, 2016). Earlier studies showed that KCNQ1OT1 was up-regulated in breast cancer and conferred to breast cancer
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