LINC00657 通过调控 microRNA-150 促进口腔鳞状细胞癌的恶性进展。
LINC00657 promotes malignant progression of oral squamous cell carcinoma via regulating microRNA-150.
机构信息
Department of Stomatology, Shaoxing Shangyu People's Hospital, Shaoxing, China.
出版信息
Eur Rev Med Pharmacol Sci. 2020 Mar;24(5):2482-2490. doi: 10.26355/eurrev_202003_20516.
OBJECTIVE
Previous studies have shown that LINC00657 is a cancer-promoting gene. However, the role of LINC00657 in oral squamous cell carcinoma (OSCC) has not been reported. This study was designed to investigate the role of LINC00657 in OSCC and its regulatory mechanism.
PATIENTS AND METHODS
Quantitative Real Time-Polymerase Chain Reaction (qPCR) was used to detect the levels of LINC00657 and microRNA-150 in 32 pairs of OSCC tissues and normal ones, and the correlation between LINC00657 and clinical indicators and OSCC patient's prognosis was analyzed. qRT-PCR further verified the levels of LINC00657 and microRNA-150 in OSCC cells. In addition, LINC00657 overexpression and knockdown models were constructed using lentivirus in OSCC cell lines Fadu and Tca8113, and Cell Counting Kit-8 (CCK-8), plate clone experiment, and 5-Ethynyl-2'-deoxyuridine (EdU) assay were carried out to evaluate the influence of LINC00657 on the biological functions of OSCC cells. Further, Luciferase reporter gene and recovery experiments were used to explore its potential mechanism.
RESULTS
qRT-PCR showed that LINC00657 expression in OSCC tissue specimens was increased in comparison to normal ones. Patients with high LINC00657 expression had higher pathological staging and lower overall survival. Besides, the cell proliferation ability of the LINC00657 silencing group was remarkably decreased, while the opposite result was observed in LINC00657 overexpression group. Subsequently, qRT-PCR demonstrated a significant decrease in microRNA-150 expression in OSCC cell lines and tissues and a negative correlation with LINC00657. Luciferase assay demonstrated that LINC00657 could be targeted by microRNA-150 in certain binding sites. In addition, cell reverse experiment also confirmed that LINC00657 and microRNA-150 can be mutually regulated, thereby jointly modulating the malignant progression of OSCC.
CONCLUSIONS
LINC00657, remarkably upregulated in OSCC tissues, showed a close association with the poor prognosis of OSCC patients. Additionally, it may accelerate the malignant progression of OSCC via regulating microRNA-150.
目的
先前的研究表明 LINC00657 是一种促进癌症的基因。然而，LINC00657 在口腔鳞状细胞癌（OSCC）中的作用尚未被报道。本研究旨在探讨 LINC00657 在 OSCC 中的作用及其调控机制。
方法
采用实时定量聚合酶链反应（qPCR）检测 32 对 OSCC 组织和正常组织中 LINC00657 和 microRNA-150 的水平，分析 LINC00657 与临床指标及 OSCC 患者预后的相关性。qRT-PCR 进一步验证了 LINC00657 和 microRNA-150 在 OSCC 细胞中的水平。此外，利用慢病毒构建了 OSCC 细胞系 Fadu 和 Tca8113 中的 LINC00657 过表达和敲低模型，通过细胞计数试剂盒-8（CCK-8）、平板克隆实验和 5-乙炔基-2'-脱氧尿苷（EdU）检测评估 LINC00657 对 OSCC 细胞生物学功能的影响。进一步利用荧光素酶报告基因和恢复实验探讨其潜在机制。
结果
qRT-PCR 显示，LINC00657 在 OSCC 组织标本中的表达高于正常组织。LINC00657 高表达的患者具有更高的病理分期和更低的总生存率。此外，沉默 LINC00657 组的细胞增殖能力显著降低，而 LINC00657 过表达组则出现相反的结果。随后，qRT-PCR 显示 OSCC 细胞系和组织中 microRNA-150 的表达显著降低，与 LINC00657 呈负相关。荧光素酶检测显示，LINC00657 可在特定结合位点被 microRNA-150 靶向。此外，细胞反向实验也证实 LINC00657 和 microRNA-150 可以相互调节，从而共同调节 OSCC 的恶性进展。
结论
LINC00657 在 OSCC 组织中显著上调，与 OSCC 患者的不良预后密切相关。此外，它可能通过调节 microRNA-150 加速 OSCC 的恶性进展。
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