Targeting NRAS Inhibits Cancer Cell Growth and Enhances Paclitaxel Sensitivity in Lung Adenocarcinoma

Abstract Lung adenocarcinoma (LUAD)poses substantial therapeutic complexities due to its resistance to first-line chemotherapic agents such as paclitaxel. This study investigated the involvement of NRAS in the development of paclitaxel resistance in LUAD. We integrated transcriptome data from TCGA and other databases while conducting in vitro experiments We also used GSEA to identify NRAS-related genes and pathways. Our findings revealed a significant up-regulation of NRAS in LUAD tissue, with higher NRAS expression correlating with adverse patient outcomes and decreased sensitivity to paclitaxel. Pathway enrichment analysis further revealed that NRAS-related genes significantly contributed to cell cycle dysregulation and impaired DNA damage repair mechanisms. Additionally, our experiments demonstrated that NRAS knockdown in LUAD cell lines exhibited increased sensitivity to paclitaxel, suggesting its potential as a viable therapeutic target. Targeting NRAS has the potential to enhance the efficacy of paclitaxel treatment in LUAD patients, offering a hopeful avenue for enhancing patient prognosis.