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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Publication Detail

Title: CCR2-dependent recruitment of macrophages by tumor-educated mesenchymal stromal cells promotes tumor development and is mimicked by TNFα.

Authors: Ren, Guangwen; Zhao, Xin; Wang, Ying; Zhang, Xin; Chen, Xiaodong; Xu, Chunliang; Yuan, Zeng-rong; Roberts, Arthur I; Zhang, Liying; Zheng, Betty; Wen, Ting; Han, Yanyan; Rabson, Arnold B; Tischfield, Jay A; Shao, Changshun; Shi, Yufang

Published In Cell Stem Cell, (2012 Dec 07)

Abstract: 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, TNFα-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.

PubMed ID: 23168163 Exiting the NIEHS site

MeSH Terms: Adaptive Immunity/immunology; Animals; Cell Communication; Cell Movement/immunology; Cell Proliferation; Cell Transformation, Neoplastic/immunology; Cell Transformation, Neoplastic/pathology*; Lymphoma/immunology*; Lymphoma/metabolism; Lymphoma/pathology*; Macrophages/metabolism; Macrophages/pathology*; Mesenchymal Stem Cells/metabolism; Mesenchymal Stem Cells/pathology*; Mice; Mice, Inbred C57BL; Monocytes/pathology; Neoplasm Transplantation; Neutrophils/pathology; Receptors, CCR2/metabolism*; Tumor Necrosis Factor-alpha/metabolism*

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