MiR-616 promotes proliferation and inhibits apoptosis in glioma cells by suppressing expression of SOX7 via the Wnt signaling pathway

Q.-L. Bai, C.-W. Hu, X.-R. Wang, J.-X. Shang, G.-F. Yin

Department of Neurosurgery, Cangzhou Central Hospital, Cangzhou, Hebei, China. bb3991@yeah.net

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• Oncology

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/β-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/β-catenin signaling. Moreover, knockdown of miR-616 may provide a potential therapeutic strategy for glioma.

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