Fibronectin-induced COX-2 mediates MMP-2 expression and invasiveness of rhabdomyosarcoma
Biochemical and Biophysical Research Communications, ISSN: 0006-291X, Vol: 318, Issue: 2, Page: 594-600
2004
- 31Citations
- 20Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations31
- Citation Indexes31
- 31
- CrossRef20
- Captures20
- Readers20
- 20
Article Description
Although accumulating evidence suggests the importance of cyclooxygenase-2 (COX-2) and prostaglandin E 2 (PGE 2 ) in the pathogenesis of many cancers, the mechanism by which this enzyme and its metabolite promote cancer progression is unknown. In this study, we investigated the role of COX-2 in fibronectin-induced up-regulation of rhabdomyosarcoma matrix metalloproteinase (MMP)-2 activity and cellular invasiveness. We tested three human rhabdomyosarcoma cell lines: RMS559, RD, and SJRH30. Cell attachment to fibronectin up-regulated both COX-2 expression and PGE 2 production and concomitantly enhanced MMP-2 activity. Exogenous PGE 2 stimulated MMP-2 promoter activity, increased MMP-2 expression, and increased cellular invasiveness. Aspirin and rofecoxib (non-selective and selective COX-2 inhibitor, respectively) each abolished fibronectin-associated induction of MMP-2 and induced dose-dependent reductions in cellular invasiveness. These data implicated a role for inducible COX-2 and PGE 2 in the regulation of rhabdomyosarcoma cellular invasiveness and MMP-2 activity.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006291X04007958; http://dx.doi.org/10.1016/j.bbrc.2004.04.070; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=2142715920&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/15120641; https://linkinghub.elsevier.com/retrieve/pii/S0006291X04007958; https://dx.doi.org/10.1016/j.bbrc.2004.04.070
Elsevier BV
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