Abstract
microRNA (miR)-6852 has been demonstrated to suppress the progression of gastric, colorectal and cervical cancer. The mechanism by which miR-6852 regulates glioma cells is yet to be elucidated. In the present study, reverse transcription-quantitative PCR analysis was used and the results demonstrated that miR-6852 expression was reduced in glioma tissues and cells. Cell counting kit-8 and transwell assay analysis indicated that proliferation, migration and invasion of A172 cells in the miR-6852 mimic group were lower than in the miR-NC group. Compared with the Inh-NC group, A172 cells of the Inh-miR-6852 group exhibited higher proliferation, migration and invasion. Additionally, the results indicated that lymphoid enhancer binding factor 1 (LEF1) was directly inhibited by miR-6852 and LEF1 expression was negatively correlated with miR-6852 expression in glioma tissues. Furthermore, the restoration of LEF1 reversed the effects of the miR-6852 mimics. The present findings suggested that miR-6852 inhibited glioma cells proliferation, migration and invasion by targeting the suppression of LEF1.
Highlights
Glioma is the most common type of central nervous system tumor in the clinical setting [1]
Results miR‐6852 expression is reduced in glioma tissues and cells
Tissues of high‐grade glioma (n=18) exhibited significantly decreased relative miR‐6852 expression when compared with tissues of low‐grade glioma (n=14; P
Summary
Glioma is the most common type of central nervous system tumor in the clinical setting [1]. Each miRNA has the potential to regulate hundreds of RNAs, and their expression is associated with tissue status and disease subtype [5]. Lv et al [4] reported that low miR‐320b expression in glioma was associated with poor patient prognosis. Patients with high‐grade glioma exhibited increased miR‐21, miR‐222 and miR‐124‐3p expression when compared with the other patients with low‐grade glioma. For high‐grade glioma, the upregulation of miR‐126 may impair the invasive ability of glioma cells by targeting KRAS, meaning miR‐126 could be an effective therapeutic target [8]. These genes are considered to be a potential biological target for glioma prognosis and treatment
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