Tumor-Associated Macrophage: Its Role in Cancer
Invasion and Metastasis
Jin-Yuan Shih, Ang Yuan1
, Jeremy J.-W. Chen, and Pan-Chyr Yang1
Department of Internal Medicine [J.-Y. Shih, P.-C. Yang] and Department of Emergency Medicine [A. Yuan], National
Taiwan University Hospital, Taipei, Taiwan; Center for Genomic Medicine, National Taiwan University College of
Medicine, Taipei, Taiwan [J. J.-W. Chen, P.-C. Yang]; Institutes of Biomedical Sciences and Molecular Biology,
National Chung-Hsing University, Taichung, Taiwan [J. J.-W. Chen]
Cancer metastasis is not exclusively regulated by the deregulation of metastasispromoting or suppressing genes in cancer cells. The interaction between cancer cells
and the stromal cells has been shown recently to promote cancer metastasis. The
macrophages within the tumor, referring to as tumour-associated macrophages
(TAMs), are the pivotal member of stromal cells. TAMs are derived from peripheral
blood monocytes recruited into the tumor. Upon activated by cancer cells, the TAMs
can release a vast diversity of growth factors, proteolytic enzymes, cytokines, and inflammatory mediators. Many of these factors are key agents in cancer metastasis.
The presence of extensive TAM infiltration has been shown to correlate with cancer
metastasis and poor prognosis in a variety of human carcinomas. TAMs promote cancer metastasis through several mechanisms including tumor angiogenesis, tumor
growth, and tumor cell migration and invasion. There are complex paracrine-signaling
networks between TAMs and cancer cells to activate each other. The colonystimulating factor 1/epidermal growth factor paracrine loop is well known in regulation
of breast cancer cells invasion. TAMs-derived proteases, such as matrix metalloproteinases, urokinase-type plasminogen activator, and cathepsin B can promote cancer
cells metastasis. The roles of TAMs in epidermal-mesenchymal transition of cancer
cells and resistance to cancer treatment are novel fields of study. On the other hand,
some investigations showed that the TAMs may play an important role in anti-tumor
activity. The control of TAMs to be pro-metastatic or tumoricidal is an important subject for cancer therapy.
Journal of Cancer Molecules 2(3): 101-106, 2006.
Keywords:
tumor-associated
macrophage
matrix metalloproteinase
invasion
metastasis
epithelial–mesenchymal
transition
Introduction
Cancer progression is a complex multi-step process that
consists of transformation, tumor growth, invasion and metastasis. Tumor invasion and metastasis are the critical
steps in determining the aggressive phenotype of human
cancers, the obstacles to the successful treatment and major
causes of cancer deaths [1]. The spread of tumor cells from
a primary tumor to secondary sites within the body is a
complicated process involving the degradation of basement
membrane, invasion of stroma, adhesion, angiogenesis, cell
proliferation, migration, and anti-apoptosis [2]. Numerous
Received 6/12/06; Revised 6/14/06; Accepted 6/14/06. 1
Correspondence: Dr. Pan-Chyr Yang, Department of Internal Medicine, or Dr. Ang Yuan, Department of Emergency Medicine, National
Taiwan University Hospital, No. 7, Chung-Shan South Road, Taipei
100, Taiwan. Phone: 886-2-2356 2905. Fax: 886-2-2358 2867. E-mail:
pcyang@ha.mc.ntu.edu.tw (Pan-Chyr Yang) or navy@ha.mc.ntu.edu.tw
(Ang Yuan) 2
Abbreviations: ECM, extracellular matrix; TAMs, tumor-associated
macrophages; NSCLC, non-small cell lung cancer; CSF-1, colonystimulating factor 1; VEGF, vascular endothelial growth factor; MIF,
macrophage migration inhibition factor; PyMT, polyoma virus middle T
oncoprotein; TNF-α, tumor-necrosis factor-α; MMPs, matrix metalloproteinases; EGF, epidermal growth factor; EMT, epithelial–mesenchymal transition.
genetic changes and a variety of positive and negative factors may be involved in the molecular basis of metastasis [3].
During cancer progression, several rounds of mutation and
selection [4]