关键词: Sp1 clinicopathological correlation miR-202 oral cancer

来  源:   DOI:10.3892/etm.2019.7603   PDF(Sci-hub)   PDF(Pubmed)

Abstract:
The current study aimed to evaluate the possible role of microRNA (miR)-202 in the development of oral cancer. First, miR-202 levels were found to be decreased in the serum and tissues of oral cancer patients compared with healthy controls. Receiver operating characteristic analysis was carried out to explore the diagnostic value of serum miR-202 for oral cancer. Overexpression of miR-202 significantly decreased the migratory capacity of SCC-9 cells, while inhibition of miR-202 markedly increased the migratory capacity of SCC-9 cells. Moreover, the invasive capacity was decreased in SCC-9 cells transfected with an miR-202 mimic. In addition, the invasive capacity was enhanced in SCC-9 cells transfected with an miR-202 inhibitor. A dual luciferase reporter assay showed that overexpression of miR-202 markedly suppressed the relative luciferase activity of the pmirGLO-SP1-3\'untranslated region. Overexpression of miR-202 suppressed the protein level of Sp1, but inhibition of miR-202 markedly enhanced the protein expression of Sp1. Inhibition of miR-202 enhanced the phosphorylation of protein kinase B. Additionally, the correlations between the expression levels of Sp1 and miR-202 and the clinicopathological factors of oral cancer were analyzed. The results showed that patients with high expression of Sp1 and miR-202 progressed to earlier clinical stages, had deeper infiltration depths and were more prone to lymph node metastasis compared with the healthy controls. In conclusion, the current study presented novel data indicating that decreased miR-202 enhanced the progression of oral cancer via Sp1.
摘要:
本研究旨在评估microRNA(miR)-202在口腔癌发生发展中的可能作用。首先,发现与健康对照相比,口腔癌患者的血清和组织中的miR-202水平降低。进行受试者工作特征分析,探讨血清miR-202对口腔癌的诊断价值。miR-202过表达显著降低SCC-9细胞的迁移能力,而抑制miR-202显著增加SCC-9细胞的迁移能力。此外,转染miR-202模拟物的SCC-9细胞的侵袭能力降低.此外,miR-202抑制剂转染的SCC-9细胞的侵袭能力增强.双荧光素酶报告基因分析显示miR-202的过表达显著抑制了pmirGLO-SP1-3'非翻译区的相对荧光素酶活性。miR-202的过表达抑制了Sp1的蛋白水平,但是miR-202的抑制显著增强了Sp1的蛋白表达。抑制miR-202增强蛋白激酶B的磷酸化。分析Sp1和miR-202表达水平与口腔癌临床病理因素的相关性。结果表明,Sp1和miR-202高表达的患者进展到更早的临床阶段,与健康对照组相比,浸润深度更深,更容易发生淋巴结转移。总之,本研究提供了新的数据,表明降低的miR-202通过Sp1促进口腔癌的进展.
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