Decoding the role of macrophage LAP3 in lung cancer – integration of single-cell technologies and machine learning reveals an orchestrating immunometabolic circuit at the tumor-epithelial interface

LAP3 appears to functionally link amino acid catabolism to immune communication in NSCLC, defining an epithelial-macrophage immunometabolic niche where metabolic activity may shape the immune contexture. Its overexpression is associated with attenuated malignant phenotypes and heightened immune engagement, suggesting a potential dual role in restraining tumor aggressiveness and fostering an immune-responsive microenvironment. While these findings support LAP3 as a candidate biomarker for patient stratification and provide a rationale for combining metabolic modulation with immunotherapy, further mechanistic and clinical validation remains necessary.