LncRNA PCAT-1 promotes the progression of osteosarcoma via miR-508-3p/ZEB1 axis

被引:11
|
作者
Chang, L. [1 ]
Jia, D-L [1 ]
Cao, C-S [1 ]
Wei, H. [2 ]
Li, Z-Q [3 ]
机构
[1] Jiyang Peoples Hosp, Dept Orthoped 2, Jinan, Peoples R China
[2] Peoples Hosp Zhangqiu Area, Ward Dept, Jinan, Peoples R China
[3] Peoples Hosp Gaomi, Dept Traumat Orthoped, Gaomi, Peoples R China
关键词
Osteosarcoma; LncRNA PCAT-1; MiR-508-3p; ZEB1; CANCER; METASTASIS; PROLIFERATION; CELLS;
D O I
10.26355/eurrev_202103_25415
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
OBJECTIVE: Osteosarcoma (OS) is an adolescent idiopathic malignancy with a poor prognosis. Accumulating evidence has verified that long non-coding RNAs (lncRNAs) were implicated in the initiation and development of various tumors. We aimed to clarify the functions and underlying mechanism of lncRNA PCAT-1 in OS progression. PATIENTS AND METHODS: RT-qPCR was performed to examine the relative expressions of PCAT-1, miR-508-3p and ZEB1 in OS tissues or cells. The proliferation capacities of OS cells with different transfection were detected by CCK-8 assays. Transwell assays were carried out to determine the functions of PCAT-1 and miR-508-3p in OS cell migration and invasion. Moreover, bioinformatical analysis and Luciferase reporter assay were applied to verify the association between PCAT-1 and miR-508-3p, miR-508-3p and ZEB1. RESULTS: Data of current study revealed that PCAT-1 was markedly upregulated in OS, which indicated poor prognosis of OS patients. CCK-8 and transwell assays indicated that PCAT-1 upregulation could promote OS cell proliferation, invasion and migration. Additionally, we found that miR-508-3p was a direct target of PCAT-1, and PCAT-1 regulated the development of OS via decreasing miR-508-3p and activating its target gene ZEB1. CONCLUSIONS: All data demonstrated that PCAT-1 promoted OS progression, and miR-5083p/ZEB1 axis was implicated in the functional roles of PCAT-1 in OS, suggesting that PCAT-1/miR-508-3p/ZEB1 might serve as candidate therapeutic targets for OS patients.
引用
收藏
页码:2517 / 2527
页数:11
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