Carcinoembryonic antigen-related cell adhesion molecule 1 negatively regulates granulocyte colony-stimulating factor production by breast tumor-associated macrophages that mediate tumor angiogenesis.
Carcinoembryonic antigen-related cell adhesion molecule 1 negatively regulates granulocyte colony-stimulating factor production by breast tumor-associated macrophages that mediate tumor angiogenesis.
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DOI：
10.1002/ijc.28036
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发表时间：
2013-07-15
影响因子：
6.4
通讯作者：
Shively, John E.
中科院分区：
文献类型：
--
作者：
Samineni, Sridhar;Zhang, Zhifang;Shively, John E.
关键词：
CEACAM1, a cell adhesion molecule expressed on epithelial cells and activated immune cells, is down-regulated in many cancers and plays a role in inhibition of inflammation in part by inhibition of G-CSF production by myeloid cells. Since macrophages are associated with a poor prognosis in breast cancer, but play important roles in normal breast, we hypothesized that CEACAM1 down-regulation would lead to tumor promotion under inflammatory conditions. Co-cultures of pro-inflammatory M1 macrophages with CEACAM1 negative MCF7 breast cells produced high levels of G-CSF (10 ng/mL) compared to CEACAM1 transfected MCF7/4S cells (1 ng/mL) or anti-inflammatory M2 macrophage co-cultures (0.5 or 0.1 ng/mL, MCF7 or MCF7/4S, respectively). The expression of CEACAM1 on M1s was much greater than for M2s and was only observed in co-cultures with either MCF7 or MCF7/4S cells. When M1 macrophages were mixed with MCF7 cells and implanted in murine mammary fat pads of NOD/SCID mice, tumor size and blood vessel density were significantly greater than MCF7 or MCF7/4S only tumors which were hardly detected after 8 weeks of growth. In contrast, M1 cells had a much reduced effect on MCF7/4S tumor growth and blood vessel density, indicating that the tumor inhibitory effect of CEACAM1 is most likely related to its anti-inflammatory action on inflammatory macrophages. These results support our previous finding that CEACAM1 inhibits both G-CSF production by myeloid cells and G-CSF stimulated tumor angiogenesis.
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