MiR-616 promotes proliferation and inhibits apoptosis in glioma cells by suppressing expression of SOX7 via the Wnt signaling pathway
MiR-616 promotes proliferation and inhibits apoptosis in glioma cells by suppressing expression of SOX7 via the Wnt signaling pathway
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DOI：
10.26355/eurrev_201712_14006
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发表时间：
2017-12-01
影响因子：
3.3
通讯作者：
Yin, G. -F.
中科院分区：
文献类型：
--
作者：
Bai, Q. -L.;Hu, C. -W.;Yin, G. -F.
目的：越来越多的证据表明miR-616在多种类型的癌症中发挥肿瘤促进作用。然而，miR-616在胶质瘤进展中的表达模式和作用仍然未知。本研究旨在揭示miR-616在胶质瘤细胞增殖中的作用及其可能的机制。患者和方法：采用实时荧光聚合酶链反应（Real-time PCR）检测miR-616在胶质瘤组织样本和胶质瘤细胞系中的表达。采用MTT增殖实验和流式细胞仪检测下调miR-616后胶质瘤细胞的凋亡和增殖情况。通过TargetScan预测miR-616的靶点，并通过荧光素酶报告基因检测进行验证。结果：miR-616在胶质瘤组织和细胞系中的表达均明显增加。MTT和流式细胞仪分析显示，下调miR-616表达可显著抑制胶质瘤细胞的增殖，促进胶质瘤细胞的凋亡。此外，使用荧光素酶测定和蛋白质印迹法证实SOX 7是胶质瘤细胞中miR-616的直接靶点。结论：miR-616在胶质瘤细胞中具有促癌作用，其致癌作用与SOX 7和Wnt/beta-catenin信号通路的调节有关。此外，miR-616的敲低可能为胶质瘤提供潜在的治疗策略。
OBJECTIVE: Accumulating evidence has indicated that miR-616 exerts tumor promoter roles in several types of cancer. However, the expression pattern and roles of miR-616 in glioma progression remain unknown. This study aimed to reveal the role of miR-616 in glioma cell proliferation and its potential mechanisms.PATIENTS AND METHODS: Real-time polymerase chain reaction was used to assay the expression of miR-616 in glioma tissue samples and glioma cell lines. MTT proliferation assay and flow cytometry analysis were performed to test the apoptosis and proliferation of glioma cell after down-regulation of miR-616. The target of miR-616 was predicted by TargetScan and confirmed by luciferase reporter assay. Changes in Wnt signaling markers expression were assessed using Western blotting.RESULTS: We found that the expression of miR-616 was increased in glioma tissues and cell lines. MTT and low cytometry analysis indicated that down-regulation of miR-616 significantly inhibited proliferation and promoted apoptosis in glioma cells. Moreover, SOX7 was confirmed to be a direct target of miR-616 in glioma cells using luciferase assay and Western blotting. Finally, it was found that down-regulation of miR-616 or upregulation of SOX7 could suppress the activity of Wnt/beta-catenin signaling in glioma cells.CONCLUSIONS: Our findings indicated that miR-616 acted as a tumor promoter in glioma, and its oncogenic roles were involved in the regulation of SOX7 and Wnt/beta-catenin signaling. Moreover, knockdown of miR-616 may provide a potential therapeutic strategy for glioma.