期刊
ONCOGENE
卷 26, 期 26, 页码 3789-3796出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.onc.1210154
关键词
breast cancer; COX-2; mouse model; MF-tricyclic; bone metastasis; cancer prevention
资金
- NIDDK NIH HHS [R21 DK067682] Funding Source: Medline
Cyclooxygenase-2 (COX- 2) is expressed in 40% of human invasive breast cancers. Bone is the predominant site of metastasis in case of breast cancer. We investigated the role of COX- 2 in a suitable mouse model of breast cancer metastasis to bone using the whole-body luciferase imaging of cancer cells. We provide several lines of evidence that COX- 2 produced in breast cancer cells is important for bone metastasis in this model including (1) COX- 2 transfection enhanced the bone metastasis of MDA-435S cells and (2) breast cancer cells isolated and cultured from the bone metastases produced significantly more prostaglandin E-2 (an important mediator of COX- 2) than the parental injected cell populations of breast cancer cells. Next, we found that a COX- 2 inhibitor, MF-tricyclic, inhibited bone metastasis caused by a bone-seeking clone both in prevention regimen (in which case mice started receiving MF-tricyclic 1 week before the injection of cancer cells) and in treatment regimen (in which case mice received MF-tricyclic after the development of bone metastasis). These studies indicate that COX- 2 produced in breast cancer cells may be vital to the development of osteolytic bone metastases in patients with breast cancer, and that COX- 2 inhibitors may be useful in halting this process.
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