The impact of COX-2 on invasion of osteosarcoma cell and its mechanism of regulation

Cancer Cell International

Lie-ming Lou¹  Fang Ji¹  Ming Cai¹  Xing Wu¹ 

[1] Department of Orthopaedics, Shanghai tenth People’s Hospital, Tongji University School of Medicine, No.301 Middle Yanchang Road, Shanghai 200072, China

关键词: Antisense oligonucleotide;    Invasion;    Osteosarcoma;    COX-2;   

Others  :  792198
DOI  :  10.1186/1475-2867-14-27

 received in 2013-08-07, accepted in 2014-03-18,  发布年份 2014

【 摘 要 】

Background

Recently, cyclooxygenase-2 (COX-2) has become an important new target in the field of tumor metastasis. However, the relationship between COX-2 gene expression and the behavior of osteosarcoma metastasis is largely unknown. The study is to investigate how antisense oligonucleotides (ODNs) of COX-2 inhibit the invasion of human osteosarcoma cell line OS-732 and their mechanism of regulation.

Methods

A COX-2 antisense oligonucleotide was designed, synthesized, and transfected into OS-732 human osteosarcoma cells. RT-PCR and western blotting were performed to determine the transfection efficiency. A modified Boyden-transwell assay was used to measure the inhibition rate of tumor cell invasion. In OS-732 cells transfected with COX-2 antisense ODNs, RT-PCR was used to examine the mRNA expression of urokinase-type plasminogen activator (uPA) and that of its receptor, uPAR.

Results

Both the mRNA and protein expression levels of COX-2 were significantly reduced when cells were transfected with COX-2 antisense ODNs, which significantly reduced the invasive ability of OS-732 cells in a dose-dependent manner. The expression levels of uPA and uPAR were also significantly reduced (p < 0.01).

Conclusion

COX-2 antisense ODNs significantly inhibited the invasion of OS-732 cells, primarily by decreasing the mRNA expression of uPA and uPAR.

【 授权许可】

   
2014 Wu et al.; licensee BioMed Central Ltd.

【 图 表 】

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