| Tumor-associated neutrophils (TANs) play important roles in the immune microenvironment of lung cancer. Through dynamic changes in their phenotypes and functions, they exert dual effects on lung cancer initiation, progression, and therapeutic response. In response to signals from the tumor microenvironment, neutrophils can polarize into the antitumor N1 phenotype or the protumor N2 phenotype. In tumor tissues, TANs often exhibit a protumor N2 phenotype and accelerate tumor invasion and metastasis by remodeling the extracellular matrix, promoting aberrant angiogenesis, and facilitating tumor immune evasion. TANs can undergo reversible phenotypic switching in response to different stimuli, which is regulated by multiple mechanisms, including transforming growth factor β, interferon β/γ, C-X-C motif chemokine receptor 2, and lipid metabolism-related signaling pathways. This review summarizes the dual roles and underlying mechanisms of TANs in lung cancer progression, with a focus on phenotypic switching, immunoregulatory functions, and the key roles of TANs in promoting angiogenesis and metastasis. It further discusses therapeutic strategies targeting TAN recruitment, phenotypic switching, metabolic reprogramming, and effector functions. In summary, modulating TAN polarization and function may provide an important point of intervention for regulating the tumor microenvironment and new directions for immunotherapy in lung cancer and other malignancies. |
