MiR-610 functions as a tumor suppressor in oral squamous cell carcinoma by directly targeting AGK

L.-X. Yao, J. Liu, L. Xu

Oral Surgery, Liaocheng People’s Hospital, Liaocheng, Shandong, China. jhssph222@sina.com

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• Oncology

OBJECTIVE: MicroRNA-610 (miR-610) functions as a tumor suppressor in various types of cancers. However, whether miR-610 acted as a functional miRNA in oral squamous cell carcinoma (OSCC) is still largely unknown. The current study was designed to explore the expression pattern and function of miR-610 in OSCC and to investigate the possible molecular mechanisms.

PATIENTS AND METHODS: Quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) was performed to detect the expression of miR-610 in OSCC tissues and cells lines. The associations between miR-610 expression and clinicopathologic features and prognosis were analyzed. Proliferation, migration, and invasion capacities of OSCC cells were assessed after overexpressing miR-610. The regulation of acylglycerol kinase (AGK) by miR-610 was confirmed by Western blotting, Dual-Luciferase reporter assays and rescue experiments.

RESULTS: We found that miR-610 expression was significantly down-regulated in both OSCC tissues and cell lines. Low miR-610 expression was associated with advanced T classification, TNM stage and poorer prognosis of OSCC patients. Functionally, the overexpression of miR-610 significantly suppressed OSCC cells proliferation, migration, invasion and EMT process. Mechanistically, AGK was confirmed to be the downstream target of miR-610 in OSCC cells. Furthermore, forced expression of AGK could rescue the inhibiting roles on cell proliferation and metastasis induced by miR-610 in OSCC cells.

CONCLUSIONS: Our findings highlight the important role of miR-610 in regulating OSCC progression by targeting AGK, indicating that miR-610 may represent a novel potential therapeutic target and prognostic marker for OSCC.

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