Cyclooxygenase-2 promotes cell proliferation, migration and invasion in U2OS human osteosarcoma cells.
- Author:
Eun Jeong LEE
1
;
Eun Mi CHOI
;
So Ra KIM
;
Jung Hea PARK
;
Hyunsook KIM
;
Kwon Soo HA
;
Young Myeong KIM
;
Sung Soo KIM
;
Myeon CHOE
;
Jong Il KIM
;
Jeong A HAN
Author Information
1. Department of Biochemistry and Molecular Biology, Kangwon National University College of Medicine, Chuncheon 200-701, Korea. gshja@kangwon.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
cell movement;
cell proliferation;
cyclooxygenase-2;
matrix metalloproteinases;
osteosarcoma
- MeSH:
Bone Neoplasms/*enzymology/pathology;
Cell Line, Tumor;
Cell Movement;
Cell Proliferation;
Cyclooxygenase 2/biosynthesis/*physiology;
Cyclooxygenase 2 Inhibitors/pharmacology;
Dinoprostone/pharmacology;
Enzyme Activation;
Humans;
Matrix Metalloproteinase 2/metabolism;
Matrix Metalloproteinase 9/metabolism;
Neoplasm Invasiveness;
Nitrobenzenes/pharmacology;
Osteosarcoma/*enzymology/pathology;
Pyrazoles/pharmacology;
Sulfonamides/pharmacology
- From:Experimental & Molecular Medicine
2007;39(4):469-476
- CountryRepublic of Korea
- Language:English
-
Abstract:
Osteosarcoma is the most common primary bone tumor, but the pathogenesis is not well understood. While cyclooxygeanse-2 (COX-2) is known to be closely associated with tumor growth and metastasis in several kinds of human tumors, the function of COX-2 in osteosarcoma is unclear. Therefore, to investigate the function of COX-2 in osteosarcoma, we established stable cell lines overexpressing COX-2 in U2OS human osteosarcoma cells. COX-2 overexpression as well as prostaglandin E(2) treatment promoted proliferation of U2OS cells. In addition, COX-2 overexpression enhanced mobility and invasiveness of U2OS cells, which was accompanied by increases of matrix metalloproteinase-2 and -9 (MMP-2 and -9) activities. Selective COX-2 inhibitors, NS-398 and celecoxib, inhibited cell proliferation and abrogated the enhanced mobility, invasiveness and MMP activities induced by COX-2 overexpression. These results suggest that COX-2 is directly associated with cell proliferation, migration and invasion in human osteosarcoma cells, and the therapeutic value of COX-2 inhibitors should be evaluated continuously.
