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

小RNA 癌症研究 抑制器 生物 转移 细胞生长 污渍 细胞培养 癌症 基因 遗传学
作者
Yao Lx,Jing Liu,Xu L
出处
期刊:PubMed 卷期号:23 (1): 187-197 被引量:5
标识
DOI:10.26355/eurrev_201901_16764
摘要

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.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.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.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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