Abstract
Distinct tumor microenvironment forms in each progression step of cancer and has diverse capacities to induce both adverse and beneficial consequences for tumorigenesis. It is now known that immune cells can be activated to favor tumor growth and progression, most probably influenced by the tumor microenvironment. Tumor-associated macrophages and tumor-associated neutrophils can exert protumoral functions, enhancing tumor cell invasion and metastasis, angiogenesis, and extracellular matrix remodeling, while inhibiting the antitumoral immune surveillance. Considering that neutrophils in inflammatory environments recruit macrophages and that recruited macrophages affect neutrophil functions, there may be various degrees of interaction between tumor-associated macrophages and tumor-associated neutrophils. Platelets also play an important role in the recruitment and regulation of monocytic and granulocytic cells in the tumor tissues, suggesting that platelet function may be essential for generation of tumor-associated macrophages and tumor-associated neutrophils. In this review, we will explore the biology of tumor-associated macrophages and tumor-associated neutrophils and their possible interactions in the tumor microenvironment. Special attention will be given to the recruitment and activation of these tumor-associated cells and to the roles they play in maintenance of the tumor microenvironment and progression of tumors.
Highlights
Cancer-related nonresolving inflammation in the tumor microenvironment (TME) is a hallmark of cancer, and cancer cells are confronted with various types of stromal and immune cells across all stages of the disease, from early carcinogenesis to tumor progression and metastasis [1, 2]
tumor-associated myeloid cells (TAMCs) result in tumorassociated macrophages (TAMs) and tumorassociated neutrophils (TANs) to be discussed in this review
Neutrophil depletion in two murine models of melanoma and fibrosarcoma reverts the increased tumor growth, angiogenesis, and metastasis observed in IFN-β-deficient mice with skewed N2 phenotypes [56], and recent review of the relationship between TAN infiltration and prognosis in human cancer demonstrates the function of TANs in murine and human tumor progression [57]
Summary
Cancer-related nonresolving inflammation in the tumor microenvironment (TME) is a hallmark of cancer, and cancer cells are confronted with various types of stromal and immune cells across all stages of the disease, from early carcinogenesis to tumor progression and metastasis [1, 2]. The components of the TME include local stromal cells, such as resident fibroblasts and macrophages, and distant recruited cells such as endothelial cells, immune cells including myeloid and lymphoid cells, bone marrow-derived precursor cells, and circulating platelets. Tumor-associated myeloid cells (TAMCs) comprise five distinct myeloid populations: tumorassociated macrophages (TAMs), monocytes expressing the angiopoietin-2 receptor Tie (Tie2-expressing monocytes or TEMs), myeloid-derived suppressor cells (MDSCs), tumorassociated neutrophils (TANs), and tumor-associated dendritic cells (Figure 1) [3]. TAMCs result in TAMs and TANs to be discussed in this review
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