Toxicogenomic Characterization of Common Genes and Signaling Pathways Associated with Multiple Toxic Metal(loid)s in Lung Cancer: A Comparative Analysis of Small-Cell and Non-Small-Cell Lung Cancer
TL;DR
Several genes and signaling pathways implicated in biological processes relevant to lung cancer, including cell survival, inflammation, oxidative stress, and angiogenesis were identified and predicted molecular interaction networks and enriched pathways differed between lung cancer subtypes, underscoring the biological heterogeneity of the disease.
Abstract
Simple Summary Exposure to toxic metals and metalloids has been associated with an increased risk of lung cancer, yet the underlying molecular mechanisms remain incompletely understood, particularly in the context of combined environmental exposure. In this study, we used publicly available toxicogenomic databases and bioinformatics tools to identify genes, interaction networks, and signaling pathways commonly associated with the investigated toxic metal(loid)s (lead, cadmium, methylmercury, arsenic, nickel, and hexavalent chromium) and lung carcinogenesis. We identified several genes and signaling pathways implicated in biological processes relevant to lung cancer, including cell survival, inflammation, oxidative stress, and angiogenesis. TP53 was consistently identified across all investigated lung cancer categories, suggesting its relevance as a common molecular link warranting further investigation. Predicted molecular interaction networks and enriched pathways differed between lung cancer subtypes, underscoring the biological heterogeneity of the disease. These findings generate hypotheses and identify candidate biomarkers for future experimental, epidemiological, and mechanistic studies of combined toxic metal(loid) exposure.