Abstract
Tumor-associated macrophages (TAMs) and tumor-associated neutrophils (TANs) have been extensively studied. Their pleotropic roles were observed in multiple steps of tumor progression and metastasis, and sometimes appeared to be inconsistent across different studies. In this review, we collectively discussed many lines of evidence supporting the mutual influence between cancer cells and TAMs/TANs. We focused on how direct interactions among these cells dictate co-evolution involving not only clonal competition of cancer cells, but also landscape shift of the entire tumor microenvironment (TME). This co-evolution may take distinct paths and contribute to the heterogeneity of cancer cells and immune cells across different tumors. A more in-depth understanding of the cancer-TAM/TAN co-evolution will shed light on the development of TME that mediates metastasis and therapeutic resistance.
Highlights
We focus on evidence showing that tumor-associated macrophages (TAMs) and tumor-associated neutrophils (TANs) directly participate in tumor initiation, proliferation, and metastasis
We named these tumors as macrophage-enriched and neutrophilenriched subtypes (MES and NES) respectively. This dichotomy may be driven by two forces: 1) the intrinsic properties of cancer cells, such as the mTOR activities and epithelial-mesenchymal transition (EMT), and 2) the mutually negative impact between TAMs and TANs
The progression of tumorigenesis and metastasis resembles the evolution of ecosystems
Summary
A study by Wang et al demonstrated that it was the neutrophils isolated from breast tumors but not from peripheral blood can significantly promote migration and invasion of a panel of breast cancer cell lines in vitro. DeNardo et al reported that CD4+ T lymphocytes skew the phenotype and effector function of CD11b+ Gr1- F4/80+ tumor associated macrophages to promote the invasion and metastasis in MMTV-PyMT mammary carcinoma model by stimulating the EGF signaling [79].
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