Journal
CELL STEM CELL
Volume 11, Issue 6, Pages 812-824Publisher
CELL PRESS
DOI: 10.1016/j.stem.2012.08.013
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Funding
- Ministry of Science and Technology of China [2010CB945600, 2011DFA30630]
- Scientific Innovation Project of the Chinese Academy of Science [XDA01040107, KSCX1-YW-22-04]
- National Science and Technology Project of China [31010103908]
- National Institutes of Health of the United States of America [GM866889, DE014913, DE019932, ES005022]
- Robert Wood Johnson Foundation [67038]
- Human Genetics Institute of New Jersey
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Mesenchymal stromal cells (MSCs) tend to infiltrate into tumors and form a major component of the tumor microenvironment. These tumor-resident MSCs are known to affect tumor growth, but the mechanisms are largely unknown. We found that MSCs isolated from spontaneous lymphomas in mouse (L-MSCs) strikingly enhanced tumor growth in comparison to bone marrow MSCs (BM-MSCs). L-MSCs contributed to greater recruitment of CD11b(+)Ly6C(+) monocytes, F4/80(+) macrophages, and CD11b(+)Ly6G(+) neutrophils to the tumor. Depletion of monocytes/macrophages, but not neutrophils, completely abolished tumor promotion of L-MSCs. Furthermore, L-MSCs expressed high levels of CCR2 ligands, and monocyte/macrophage accumulation and L-MSC-mediated tumor promotion were largely abolished in CCR2(-/-) mice. Intriguingly, TNF alpha-pretreated BM-MSCs mimicked L-MSCs in their chemokine production profile and ability to promote tumorigenesis of lymphoma, melanoma, and breast carcinoma. Therefore, our findings demonstrate that, in an inflammatory environment, tumor-resident MSCs promote tumor growth by recruiting monocytes/macrophages.
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