Abstract
AbstractThe dysregulated lncRNA play essential roles in glioma development. This study aimed to investigate the role and mechanism of lncRNA potassium voltage-gated channel subfamily Q member 1 opposite strand/ antisense transcript 1 (KCNQ1OT1) in glioma progression. Tumor tissues and adjacent normal samples were collected from 30 glioma patients. The expression levels of lncRNA KCNQ1OT1, microRNA (miR)-338-3p and ribonucleotide reductase M2 (RRM2) were detected by quantitative real-time polymerase chain reaction or western blot analyses. Levels of cell viability, apoptosis, cell migration and invasion in glioma cell lines were determined using cell counting kit-8, flow cytometry with annexin V-FITC and trans-well assays, respectively. The role of KCNQ1OT1 in glioma development in vivo was investigated using a xenograft model. The target association between miR-338-3p and KCNQ1OT1 or RRM2 was validated by luciferase reporter assay. The results found that expression of KCNQ1OT1 was enhanced in glioma tissues and cells, and KCNQ1OT1 knockdown inhibited cell viability, migration and invasion, and xenograft tumor growth, but promoted apoptosis. miR-338-3p was targeted via KCNQ1OT1 and could reverse the effect of KCNQ1OT1 on glioma progression. RRM2 was targeted via miR-338-3p and attenuated the suppressive effect of miR-338-3p on glioma cell viability, migration and invasion. Besides, KCNQ1OT1 overexpression increased RRM2 expression, and this event was weakened via miR-338-3p up-regulation. In conclusion, the present finding suggest that silencing of KCNQ1OT1 can suppress the development and progression of glioma by up-regulating miR-338-3p and down-regulating RRM2.
Highlights
Glioma accounts for about 30% of primary brain tumors with high morbidity and mortality in adults and children [1,2,3]
Cell viability was measured via Cell counting kit-8 (CCK8) assay, and the data of CCK8 assay suggested that knockdown of KCNQ1OT1 decreased the viability of A172 and U251 cells at 72 h (Figure 2C and 2D)
The mechanisms underpinning the involvement of long noncoding RNAs (lncRNAs) KCNQ1OT1 in glioma progression remain to be elucidated
Summary
Glioma accounts for about 30% of primary brain tumors with high morbidity and mortality in adults and children [1,2,3]. Liang et al reported that knockdown of lncRNA paternally expressed gene 10 (PEG10) decreased proliferation, migration and invasion of glioma [8]. Liu et al suggested the involvement of small nucleolar RNA host gene 20 (SNHG20) as an oncogenic lncRNA in glioma that promotes cell proliferation [9]. LncRNA potassium voltage-gated channel subfamily Q member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) has been identified as an oncogenic lncRNA that plays a role in promoting progression of cancers, including hepatocellular carcinoma, breast cancer, cholangiocarcinoma and non-small-cell lung carcinoma [11,12,13,14]. Additional studies have shown that knockdown of KCNQ1OT1 repressed proliferation, migration and invasion of glioma by activating the miR-370/CCNE2 axis [15]. The mechanism underpinning the role of KCNQ1OT1 in glioma progression appears to be complex and warrants further investigation
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