کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1930577 | 1050518 | 2011 | 6 صفحه PDF | دانلود رایگان |
In the evolution of cancer, tumor necrosis factor-alpha (TNF-α) plays a paradoxical role. High doses induce significant anticancer effects, but conversely, physiologic and pathologic levels of TNF-α may be involved in cancer promotion, tumor growth, and metastasis.Infliximab is a chimeric murine monoclonal antibody that binds with high affinity to soluble and membrane TNF-α and inhibits binding of TNF-α to its receptors. In the present study, we investigated the effect of infliximab, a TNF-α antagonist, on breast cancer aggressiveness and bone metastases.Infliximab greatly reduced cell motility and bone metastases in a metastatic breast cancer cell line, MDA-MB-231. The mechanism of bone metastasis inhibition involved decreased expression of CXC chemokine receptor 4 (CXCR4) and increased expression of decorin, which is the prototype of an expanding family of small leucine-rich proteoglycans. These results suggest a novel role for TNF-α inhibition in the reduction or prevention of bone metastases in this breast cancer model. Our study suggests that inhibition of TNF-α using infliximab may become a preventive therapeutic option for breast cancer.
► Infliximab, TNF-α inhibitor, reduced cell motility and bone metastases in breast cancer cell.
► The mechanism of bone metastasis inhibition involved decreased expression of CXCR4 (chemokine receptor).
► Another mechanism involved increased expression of decorin (small leucine-rich proteoglycans).
► Inhibition of TNF-α using infliximab may become a preventive therapeutic option for breast cancer.
Journal: Biochemical and Biophysical Research Communications - Volume 407, Issue 3, 15 April 2011, Pages 525–530