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Cancers 2017, 9(6), 68; doi:10.3390/cancers9060068

Promotion of Tumor Invasion by Tumor-Associated Macrophages: The Role of CSF-1-Activated Phosphatidylinositol 3 Kinase and Src Family Kinase Motility Signaling

School of Biomedical Sciences, The University of Western Australia, 35 Stirling Highway, Crawley, WA 6009, Australia
Current address: University of Minnesota, Cancer Cardiology Research Building, Suite 3-2406, 2231 6th Street SE, Minneapolis, MN 55455, USA
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Author to whom correspondence should be addressed.
Academic Editor: Marco Falasca
Received: 2 May 2017 / Revised: 8 June 2017 / Accepted: 12 June 2017 / Published: 18 June 2017
(This article belongs to the Special Issue PI3K/PDK1/Akt Pathways in Cancer)
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Abstract

Macrophages interact with cells in every organ to facilitate tissue development, function and repair. However, the close interaction between macrophages and parenchymal cells can be subverted in disease, particularly cancer. Motility is an essential capacity for macrophages to be able to carry out their various roles. In cancers, the macrophage’s interstitial migratory ability is frequently co-opted by tumor cells to enable escape from the primary tumor and metastatic spread. Macrophage accumulation within and movement through a tumor is often stimulated by tumor cell production of the mononuclear phagocytic growth factor, colony-stimulating factor-1 (CSF-1). CSF-1 also regulates macrophage survival, proliferation and differentiation, and its many effects are transduced by its receptor, the CSF-1R, via phosphotyrosine motif-activated signals. Mutational analysis of CSF-1R signaling indicates that the major mediators of CSF-1-induced motility are phosphatidyl-inositol-3 kinase (PI3K) and one or more Src family kinase (SFK), which activate signals to adhesion, actin polymerization, polarization and, ultimately, migration and invasion in macrophages. The macrophage transcriptome, including that of the motility machinery, is very complex and highly responsive to the environment, with selective expression of proteins and splice variants rarely found in other cell types. Thus, their unique motility machinery can be specifically targeted to block macrophage migration, and thereby, inhibit tumor invasion and metastasis. View Full-Text
Keywords: macrophage motility; colony-stimulating factor-1; phosphatidyl-inositol-3-kinase; Src family kinases; paracrine interaction macrophage motility; colony-stimulating factor-1; phosphatidyl-inositol-3-kinase; Src family kinases; paracrine interaction
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MDPI and ACS Style

Dwyer, A.R.; Greenland, E.L.; Pixley, F.J. Promotion of Tumor Invasion by Tumor-Associated Macrophages: The Role of CSF-1-Activated Phosphatidylinositol 3 Kinase and Src Family Kinase Motility Signaling. Cancers 2017, 9, 68.

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