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RETRACTED: MicroRNA-708 inhibits the proliferation and invasion of osteosarcoma cells by directly targeting ZEB1 (Retracted article. See vol. 27, 2023)
被引:6
|作者:
He, Jun
[1
]
Xiang, Deng
[1
]
Lin, Yanshui
[1
]
机构:
[1] Chengdu Med Coll, Affiliated Hosp 1, Dept Orthoped, 278 Baoguang St, Chengdu 610500, Sichuan, Peoples R China
关键词:
osteosarcoma;
microRNA-708;
zinc finger E-box binding homeobox 1;
proliferation;
invasion;
MESENCHYMAL TRANSITION;
METASTASIS;
EXPRESSION;
MECHANISMS;
CARCINOMA;
APOPTOSIS;
PROMOTES;
CANCER;
ACTS;
D O I:
10.3892/mmr.2019.10013
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
Numerous microRNAs (miRNAs) have been identified as aberrantly expressed in osteosarcoma (OS). miRNAs serve important roles in the pathogenesis of OS as oncogenes or tumor suppressors. Recent studies revealed that miR-708-5p (miR-708) was dysregulated in various types of human cancer; however, its roles and underlying molecular mechanisms in OS remain unknown. Therefore, the present study aimed to determine miR-708 expression in OS, investigate the roles of miR-708 in the progression of OS and reveal the potential mechanisms involved. It was demonstrated using reverse transcription-polymerase chain reaction that miR-708 was downregulated in OS tissues and cell lines. Cell Counting Kit-8 and Transwell assays revealed that miR-708 overexpression suppressed the proliferation and invasion of OS cells in vitro. Additionally, zinc finger E-box binding homeobox 1 (ZEB1) was validated as a direct target gene of miR-708 in OS cells. ZEB1 was upregulated in OS tissues; elevated ZEB1 expression was negatively correlated with the levels of miR-708 expression. Rescue experiments indicated that ZEB1 reintroduction significantly counteracted the inhibitory effects of miR-708 overexpression on the proliferation and invasion of OS cells. The findings may improve understanding of the roles of miR-708 in the development of OS, and suggest that miR-708 may be a potential novel therapeutic target in the treatment of patients with this disease.
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页码:3948 / 3954
页数:7
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