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Cited by 1,188

The DOI matches its Crossref record.

A Paracrine Loop between Tumor Cells and Macrophages Is Required for Tumor Cell Migration in Mammary Tumors

Wyckoff, Jeffrey, Wang, Weigang, Lin, Elaine Y., Wang, Yarong, Pixley, Fiona, Stanley, E. Richard, Graf, Thomas, Pollard, Jeffrey W., Segall, Jeffrey, Condeelis, John·2004·Cancer Research
DOI 10.1158/0008-5472.can-04-1449
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Abstract

Invasion of tumor cells into the surrounding connective tissue and blood vessels is a key step in the metastatic spread of breast tumors. Although the presence of macrophages in primary tumors is associated with increased metastatic potential, the mechanistic basis for this observation is unknown. Using a chemotaxis-based in vivo invasion assay and multiphoton-based intravital imaging, we show that the interaction between macrophages and tumor cells facilitates the migration of carcinoma cells in the primary tumor. Gradients of either epidermal growth factor (EGF) or colony-stimulating factor 1 (CSF-1) stimulate collection into microneedles of tumor cells and macrophages even though tumor cells express only EGF receptor and macrophages express only CSF-1 receptor. Intravital imaging shows that macrophages and tumor cells migrate toward microneedles containing either EGF or CSF-1. Inhibition of either CSF-1– or EGF-stimulated signaling reduces the migration of both cell types. This work provides the first direct evidence for a synergistic interaction between macrophages and tumor cells during cell migration in vivo and indicates a mechanism for how macrophages may contribute to metastasis.

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Metadata

Authors
Wyckoff, J., Wang, W., Lin, E. Y., Wang, Y., Pixley, F., Stanley, E. R., Graf, T., Pollard, J. W., Segall, J., & Condeelis, J.
Venue
Cancer Research
Publisher
American Association for Cancer Research (AACR)
Published
2004-10-01
Volume
64
Issue
19
Pages
7022-7029
ISSN
  • 0008-5472 (ISSN-L)
  • 1538-7445
DOI
10.1158/0008-5472.can-04-1449
OpenAlex
W2000217512
Cited by
1,188
References
0
FWCI
11.01
Type
journal article
Language
en
Open access
closed

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