Opsin3 regulates cell proliferation, migration, and apoptosis in lung adenocarcinoma via GPX3 pathway.

Despite recent progress in understanding lung adenocarcinoma (LUAD) and the emergence of new therapeutic strategies, LUAD continues to be one of the deadliest lung cancer types, with a five-year survival rate of under 5%. Opsin3 (OPN3), a member of the G protein-coupled receptor superfamily, has been linked to various cancer-related processes, including tumor progression and therapy resistance. However, its specific role in LUAD remains insufficiently investigated. This study aimed to explore OPN3's regulatory functions in LUAD and evaluate its potential as a therapeutic target. OPN3 expression in LUAD cells was assessed using quantitative PCR, Western blotting, and immunohistochemistry. The effects of OPN3 on cell migration and invasion were evaluated through wound healing and transwell assays. Additionally, the influence of OPN3 on cell cycle progression and signaling pathways in vivo-critical for cellular responses to external stimuli-was examined. Pathway enrichment analysis revealed significant disruption of genes associated with glutathione metabolism. Notably, a strong correlation between OPN3 expression and the regulation of Glutathione Peroxidase 3 (GPX3), a key enzyme in this metabolic pathway, was identified. Our results demonstrate that OPN3 is markedly overexpressed in LUAD tissues relative to normal lung tissues. Silencing OPN3 via siRNA significantly diminished the malignant features of LUAD cells, including proliferation, migration, and invasion. In contrast, OPN3 overexpression enhanced these malignant characteristics, indicating its involvement in tumor progression. Moreover, an inverse relationship between OPN3 expression and GPX3 levels was observed, suggesting that OPN3 may drive LUAD progression through the GPX3 pathway. This study offers new insights into the function of OPN3 in LUAD and suggests that targeting the OPN3-GPX3 axis could provide a promising therapeutic strategy for LUAD patients.