Abstract
Recent preclinical/clinical studies have underscored the significant impact of tumor microenvironment (TME) on tumor progression in diverse scenarios. Highly heterogeneous and complex, the tumor microenvironment is composed of malignant cancer cells and non-malignant cells including endothelial cells, fibroblasts, and diverse immune cells. Since immune compartments play pivotal roles in regulating tumor progression via various mechanisms, understanding of their multifaceted functions is crucial to developing effective cancer therapies. While roles of lymphoid cells in tumors have been systematically studied for a long time, the complex functions of myeloid cells have been relatively underexplored. However, constant findings on tumor-associated myeloid cells are drawing attention, highlighting the primary effects of innate immune cells such as monocytes and neutrophils in disease progression. This review focuses on hitherto identified contextual developments and functions of monocytes and neutrophils with a special interest in solid tumors. Moreover, ongoing clinical applications are discussed at the end of the review.
Highlights
Reviewed by: Markus Munder, Johannes Gutenberg University Mainz, Germany Raymond B
This review focuses on hitherto identified contextual developments and functions of monocytes and neutrophils with a special interest in solid tumors
CSF-1R interacts with its ligands CSF-1 (M-CSF) and IL-34 to regulate the development of monocytes in the bone marrow [1, 2]
Summary
Reviewed by: Markus Munder, Johannes Gutenberg University Mainz, Germany Raymond B. IL-6IL-6R interaction promotes VEGF-A secretion from classical monocytes and activates the STAT3 signaling pathway in cancer cells, which enhances tumor cell proliferation in pancreatic ductal adenocarcinoma (PDAC) [50,51,52,53]. In B16F10 melanoma and MMTV-PyMT spontaneous mammary carcinoma, non-classical monocytes play a pivotal role in engulfing tumor material in the lung and attenuating tumor metastasis and activating NK cells [17, 35].
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