Cyclooxygeanse-2 promotes metastasis in osteosarcoma

Cancer Cell International

Bing Liu²  Liyan Qu¹ 

[1]Clinical Laboratory Centre, Binjiang Hospital of Hangzhou, Hangzhou, Zhejiang, China

[2]Department of Orthopedics, 2nd Affiliated Hospital, School of Medicine, Zhejiang University, #88 Jie Fang Road, Hangzhou 310009, Zhejiang, People’s Republic of China

关键词: Osteosarcoma;    Metastasis;    COX-inhibitors;    COX-2;   

Others  :  1219324
DOI  :  10.1186/s12935-015-0220-2

 received in 2014-08-18, accepted in 2015-06-23,  发布年份 2015

【 摘 要 】

Cyclooxygenase-2 (COX-2), an inducible form of the enzyme that catalyzes the first step in the synthesis of prostanoids, is associated with carcinogenesis, which is suspected to promote angiogenesis and tissue invasion of tumors and resistance to apoptosis. COX-2 is also involved in metastasis and poor prognosis of cancer. Osteosarcoma with COX-2 positivity is from 67 to 92 %. COX-2-positive rate in metastatic lesions was greater than that of biopsy and/or resected samples of the primary site in osteosarcoma. And, what role does COX-2 play in osteosarcoma metastasis? Genetic studies support a cause-effect connection between COX-2 and tumorigenesis. COX-2 expression had a poor prognosis with regard to metastasis, and patients with increased COX-2 expression in lung metastases died of the disease. COX-2 expression has also been established as a marker in human osteosarcoma, and COX-2 inhibition has been suggested as a possible way of improving therapeutic outcome. In addition, COX-inhibitors inhibit the tumor initiation, matrix metalloproteinases (MMPs), cell differentiation and T cell proliferation and suppression of the antitumor activity of natural killer cells and macrophages, angiogenic mechanism. Therefore, we can exert the COX-inhibitors to potentialize the effects of chemotherapeutic agents, and reverse the metastasis in osteosarcoma to facilitate the patient who may benefit from addition of COX-inhibitors to standard cytotoxic therapy.

【 授权许可】

   
2015 Qu and Liu.

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