Oral Surgery, Liaocheng People's Hospital, Liaocheng, Shandong, China.
Eur Rev Med Pharmacol Sci. 2019 Jan;23(1):187-197. doi: 10.26355/eurrev_201901_16764.
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.
MicroRNA-610（miR-610）在多种类型的癌症中作为肿瘤抑制因子发挥作用。然而，miR-610 是否在口腔鳞状细胞癌（OSCC）中作为功能性 miRNA 发挥作用仍知之甚少。本研究旨在探讨 miR-610 在 OSCC 中的表达模式和功能，并研究其可能的分子机制。
采用定量逆转录-聚合酶链反应（qRT-PCR）检测 OSCC 组织和细胞系中 miR-610 的表达。分析 miR-610 表达与临床病理特征和预后的关系。过表达 miR-610 后评估 OSCC 细胞的增殖、迁移和侵袭能力。通过 Western blot、双荧光素酶报告基因检测和挽救实验证实酰基甘油激酶（AGK）受 miR-610 的调控。
我们发现 miR-610 在 OSCC 组织和细胞系中的表达均显著下调。低 miR-610 表达与 OSCC 患者的 T 分类、TNM 分期和预后不良相关。功能上，miR-610 的过表达显著抑制了 OSCC 细胞的增殖、迁移、侵袭和 EMT 过程。机制上，AGK 被确认为 OSCC 细胞中 miR-610 的下游靶标。此外，强制表达 AGK 可挽救 miR-610 对 OSCC 细胞增殖和转移的抑制作用。
我们的研究结果强调了 miR-610 通过靶向 AGK 调节 OSCC 进展的重要作用，表明 miR-610 可能代表 OSCC 的一种新的潜在治疗靶点和预后标志物。
