ABSTRACT: RNA-seq data were generated to characterize global gene expression differences, identify key differentially expressed genes, and explore the associated biological pathways and molecular mechanismsThis study aimed to investigate the expression and function of NAD(P)H:quinone oxidoreductase 1 (NQO1) during glycidyl methacrylate (GMA)-induced malignant transformation of lung epithelial cells and its association with oxidative stress-related signaling pathways.BEAS-2B cells were chronically exposed to GMA to establish a malignant transformation model (GMA-T50). Cell migration, invasion, and proliferation were assessed using wound-healing, Transwell, soft agar, and colony formation assays. Tumorigenicity was evaluated in nude mice with histopathology and immunohistochemistry. Transcriptomic sequencing and bioinformatics analyses were used to identify key molecules. NQO1 expression was measured by reverse transcription quantitative PCR and Western blotting. After siRNA-mediated NQO1 knockdown, proliferation, migration, invasion, and apoptosis were analyzed. Intracellular reactive oxygen species were detected using 2′,7′-dichlorodihydrofluorescein diacetate, and the nuclear factor erythroid 2–related factor 2/heme oxygenase-1 signaling pathway was examined, with N-acetyl-L-cysteine used to modulate oxidative stress. Long-term GMA exposure induced stable malignant phenotypes with increased migration, invasion, and proliferation and tumor formation in vivo. NQO1 mRNA and protein levels were markedly upregulated in transformed cells . NQO1 knockdown significantly suppressed proliferation, migration, and invasion and promoted apoptosis . GMA increased ROS and upregulated Nrf2, HO-1, and NQO1, whereas NAC reduced ROS and downregulated pathway proteins. NQO1 was also highly expressed in lung adenocarcinoma cells and tissues , suggesting that it may promote malignant progression through the ROS-mediated Nrf2/HO-1 pathway.
