MiR-650 inhibits the progression of glioma by targeting FAM83F

L. Xu, Q.-W. Yu, S.-Q. Fang, Y.-K. Zheng, J.-C. Qi

Department of Neurosurgery, Central People’s Hospital of Zhanjiang, Zhanjiang, China. xuliniu@126.com

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• Oncology

OBJECTIVE: The aim of this study was to explore whether miR-650 could inhibit the proliferation of glioma by regulating FAM83F and to investigate the specific role of miR-650 in glioma occurrence.

PATIENTS AND METHODS: The expression of FAM83F in tumor or para-cancerous tissues of 24 glioma patients was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Meanwhile, FAM83F expression in 6 glioma cell lines (LN229, U87, U251, LN308, SNB19 and H4) was also detected. Subsequently, the proliferation of glioma cells transfected with miR-650 mimics was evaluated by cell counting kit-8 (CCK-8) and EDU (5-ethynyl-2’-deoxyuridine) assay, respectively. In addition, Luciferase reporter gene assay and rescue experiment were applied to verify the relationship between miR-650 and FAM83F.

RESULTS: MiR-650 expression in glioma tissues was significantly decreased, while the expression of FAM83F was remarkably upregulated. This indicated that the level of miR-650 was negatively correlated with that of FAM83F. Similar results were obtained in glioma cells. We then transfected miR-650 mimics into LN229 and U251 cells, and found that the expression of miR-650 was significantly upregulated. Meanwhile, the viability of cells significantly decreased. In addition, the interaction between miR-650 and FAM83F was verified by Luciferase reporter gene assay. Rescue experiments showed that miR-650 could inhibit cell proliferation by targeting FAM83F.

CONCLUSIONS: MiR-650 was lowly expressed in glioma tissues, which could promote cell proliferation through up-regulating the expression of FAM83F.

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