Fig. 2
From: The roles of tissue resident macrophages in health and cancer
Dynamic crosstalk between pro- and antitumorigenic alveolar macrophages (AMs) and tumor cells in primary and metastatic cancers. In primary tumors, AMs expressing P16 and CXCR1 suppress CTL response and promoting the progression of lung tumor via the ROS, BACH1, PDLIM2 and STAT3 signaling pathway; Upregulation of INHBA expression in AMs leads to the secretion of activin A, which inhibits the proliferation of lung cancer cells. Additionally, AMs-derived extracellular vesicles containing SOCS3 suppresses STAT3 activation in cancer cells leading to inhibits the proliferation and survival of lung adenocarcinoma cells. Upregulation of pro-inflammatory genes, such as IL-12β, IL-1α, and IL-1β, and also anti-inflammatory genes, including Smad3 of the TGF-β signaling pathway, and downregulation of Smad7. During cancer metastasis, AMs are recruited from MO-MDSCs through the CXCL10-CXCR3 and TLR4-CCL12 axis, and contributing to the metastatic progression through the Wnt/β-catenin/TNF-α axis