Long noncoding RNA UCA1 promotes cell growth, migration, and invasion by targeting miR-143-3p in oral squamous cell carcinoma

被引:26
|
作者
Duan, Qingyun [1 ,2 ]
Xu, Mei [3 ]
Wu, Meng [4 ]
Zhang, Xiong [2 ]
Gan, Min [2 ]
Jiang, Hongbing [1 ,5 ]
机构
[1] Nanjing Med Univ, Jiangsu Key Lab Oral Dis, Nanjing, Jiangsu, Peoples R China
[2] Zhejiang Univ, Coll Med, Dept Oral & Maxillofacial Surg, Affiliated Hangzhou Peoples Hosp 1, Hangzhou, Zhejiang, Peoples R China
[3] Hangzhou Jianggan Dist Peoples Hosp, Dept Ophtalmol, Hangzhou, Zhejiang, Peoples R China
[4] Nanjing Med Univ, Affiliated Huaian 1 Peoples Hosp, Dept Oral & Maxillofacial Surg, Huaian, Jiangsu, Peoples R China
[5] Nanjing Med Univ, Affiliated Stomatol Hosp, Dept Oral & Maxillofacial Surg, 136 Hanzhong Rd, Nanjing 210029, Jiangsu, Peoples R China
来源
CANCER MEDICINE | 2020年 / 9卷 / 09期
关键词
miR-143-3p; MYO6; oral squamous cell carcinoma; UCA1; INHIBITS PROLIFERATION; COLORECTAL-CANCER; MESENCHYMAL-TRANSITION; PROGRESSION; KNOCKDOWN; SUPPRESSES; NETWORKS;
D O I
10.1002/cam4.2808
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background The long noncoding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) is dysregulated in many types of tumors; however, its role in oral squamous cell carcinoma (OSCC) remains unclear. This study aims to determine the effect of lncRNA UCA1 on OSCC. Methods Fifty-six paired OSCC and adjacent nontumorous tissues were collected and the levels of UCA1, miR-143-3p, and MYO6 in the tissues were evaluated by qRT-PCR. In in vitro experiments, cell viability, migration, and invasion were measured by, respectively, performing CCK-8, wound healing, and transwell assays. The target relationships among UCA1, miR-143-3p, and MYO6 were verified by dual-luciferase assay. Western blot and immunohistochemistry were carried out to determine the protein levels. Xenograft mouse model was established to explore the effects of UCA1 in vivo. Results Levels of UCA1 and MYO6 were increased significantly in OSCC, while the level of miR-143-3p was decreased compared with the adjacent nontumorous tissues. UCA1 promoted OSCC cell growth, migration, and invasion both in vitro and in vivo, while miR-143-3p reversed the progression. MYO6 was validated as a target for miR-143-3p, and MYO6 overexpression reversed the effects of miR-143-3p mimic on OSCC cells. Conclusion LncRNA UCA1 contributes to the proliferation and metastasis of OSCC cells by targeting miR-143-3p and upregulating its downstream gene MYO6. UCA1 could serve as a promising novel target therapy for treatment of OSCC.
引用
收藏
页码:3115 / 3129
页数:15
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