The molecular intersections of pulmonary fibrosis and lung cancer

Pulmonary fibrosis (PF) and lung cancer (LC) are devastating pulmonary diseases that frequently coexist, and there is accumulating evidence that highlights the convergence of key molecular pathways contributing to both fibrogenesis and tumorigenesis. This review examines pivotal molecular targets, including the proteasome, programmed death-ligand 1 (PD-L1), poly(ADP-ribose) polymerase (PARP), breast cancer susceptibility gene (BRCA), transforming growth factor-beta (TGF-β), hypoxia-inducible factor (HIF), Yes-associated protein (YAP), and β-catenin, that play central roles in the initiation and progression of both PF and LC. We provide mechanistic insights into the dual roles of these molecules, emphasizing how certain pathways promote both fibrotic remodeling and malignant transformation. Their divergent effects across pathological contexts underscore the need for precision medicine approaches. Leveraging these convergent mechanisms offers a unique opportunity for cross-disease therapeutic development.