NPM1 Serves as a Tumor-Promoting Gene in Lung Adenocarcinoma by Regulating Glycolysis

Abstract

Background: The role of Recombinant Nucleophosmin 1 (NPM1) in the development of lung adenocarcinoma (LUAD) has been recognized, however, the precise mechanism underlying this involvement remains unclear. Therefore, this study aimed to assess the mechanism of NPM1 in LUAD progression. Methods: Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting assays were used to detect the expression level of NPM1. Furthermore, Cell Counting Kit-8 (CCK-8) assay, Transwell migration, Transwell invasion, and flow cytometry assays were conducted to evaluate the role of NPM1 in the proliferation, migration, invasion, and apoptosis in LUAD cell lines. Moreover, glycolysis-related indicators were determined using corresponding kits. Additionally, the mechanism of NPM1 involvement was further evaluated through NPM1 silencing experiments. Results: NPM1 was upregulated in two human LUAD cell lines (p < 0.001). Glycolysis was enhanced in LUAD cell lines (p < 0.05). After inhibiting the expression of NPM1, the proliferation, migration, and invasion were significantly reduced in LUAD cell lines but the apoptosis was increased (p < 0.05). Furthermore, a substantial reduction in glycolytic flux and an elevation in mitochondrial respiration were observed (p < 0.05). Conclusion: These findings reveal that NPM1 promotes LUAD progression by mediating glycolysis, offering a novel therapeutic target for treating LUAD.