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Type: Journal article
Title: Promotion of tumor invasion by tumor-associated macrophages: the role of CSF-1-activated phosphatidylinositol 3 kinase and Src family kinase motility signaling
Author: Dwyer, A.R.
Greenland, E.L.
Pixley, F.J.
Citation: Cancers, 2017; 9(6):68
Publisher: MDPI AG
Issue Date: 2017
ISSN: 2072-6694
Statement of
Amy R. Dwyer, Eloise L. Greenland and Fiona J. Pixley
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.
Keywords: macrophage motility; colony-stimulating factor-1; phosphatidyl-inositol-3-kinase; Src family kinases; paracrine interaction
Description: Published: 18 June 2017
Rights: © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (
RMID: 1000006528
DOI: 10.3390/cancers9060068
Grant ID:
Appears in Collections:Medicine publications

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