Breaking the vicious cycle between breast cancer cells and tumor-associated macrophages

被引：24

作者：

Su, Shicheng ^{[1
,2
,3
]}

Wu, Wei ^{[1
,2
,3
]}

He, Chonghua ^{[1
,2
,3
]}

Liu, Qiang ^{[1
,2
,3
]}

Song, Erwei ^{[1
,2
,3
]}

机构：

[1] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Med Res Ctr, Guangdong Prov Key Lab Malignant Tumor Epigenet &, Guangzhou 510275, Guangdong, Peoples R China

[2] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Breast Tumor Ctr, Guangzhou 510275, Guangdong, Peoples R China

[3] Sun Yat Sen Univ, Sun Yat Sen Mem Hosp, Dept Oncol, Guangzhou 510275, Guangdong, Peoples R China

来源：

ONCOIMMUNOLOGY | 2014年 / 3卷 / 08期

关键词：

EMT; humanized mice; tumor-associated macrophages; tumor metabolism; METASTASIS; VACCINE;

D O I：

10.4161/21624011.2014.953418

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

We recently identified a vicious cycle between granulocyte macrophage colony stimulating factor (GM-CSF) arising from breast cancer cells that have undergone epithelial-mesenchymal transition (EMT) and the tumor-associated macrophage (TAM)-derived chemokine CCL18, a signaling loop that promotes tumor metastasis. Tumor-derived lactate skews GM-CSF-activated macrophages to an anti-inflammatory and immunosuppressive M2 phenotype, suggesting that breaking this cycle in combination with glycolysis inhibitors may inhibit tumor development.

引用

页数：3

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