miRNA-101 Targets TGF-βR1 to Retard the Progression of Oral Squamous Cell Carcinoma

被引:22
|
作者
Wang, Yong [1 ,2 ]
Jia, Rui-Zhi [1 ,2 ]
Diao, Shu [1 ,2 ]
He, Jun [3 ]
Jia, Li [3 ]
机构
[1] Capital Med Univ, Beijing Stomatol Hosp, Dept Pediat Dent, Beijing, Peoples R China
[2] Capital Med Univ, Sch Stomatol, Beijing, Peoples R China
[3] Inst Dis Control & Prevent PLA, Evaluat & Res Ctr Toxicol, 27 Taiping Rd, Beijing 100071, Peoples R China
关键词
miR-101; Transforming growth factor-beta receptor 1 (TGF-beta R1); Oral squamous cell carcinoma (OSCC); Growth; Metastasis; THERAPEUTIC TARGET; CANCER STATISTICS; SIGNALING PATHWAY; NONCODING RNA; PROLIFERATION; PROMOTES; GROWTH; ANGIOGENESIS; EXPRESSION; SIGNATURES;
D O I
10.3727/096504019X15761480623959
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Despite the considerable knowledge on the involvement of microRNA-101 (miR-101) in the evolution of oral squamous cell carcinoma (OSCC), the underlying mechanisms remain obscure. In this study, miR-101 expression was markedly downregulated in the OSCC cell lines and tissues. Cell counting kit-8 (CCK-8), ethynyl deoxyuridine (EdU), and colony formation assays showed that miR-101 inhibited the proliferation of OSCC cells. Flow cytometry and caspase 3 activity assays indicated that miR-101 induced OSCC cell apoptosis. Transwell assays demonstrated that this miRNA also repressed OSCC cell migration and invasion. Moreover, tube formation assay showed that miR-101 abated the proangiogenesis of OSCC cells. Dual-luciferase reporter assay confirmed that miR-101 directly targeted transforming growth factor-beta receptor 1 (TGF-beta R1) in OSCC. Ectopic expression of TOF-beta R1 counteracted the effects of miR-101 on the OSCC cell characteristics. Thus, miR-101 significantly abolished the proliferation, motility, and proangiogenesis of OSCC cells and induced their apoptosis by targeting TGF-beta R1. These results imply the potential application of miR-101 in OSCC treatment.
引用
收藏
页码:203 / 212
页数:10
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