ArticleClinics (Sao Paulo, Brazil)2026
NRP1 silencing induces ROS-mediated cell cycle arrest and mitochondrial apoptosis in non-small cell lung cancer via upregulation of AGER.
Article in Clinics (Sao Paulo, Brazil), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveThe specific role of Neuropilin-1 (NRP1) and its link to oxidative stress in Non-Small Cell Lung Cancer (NSCLC) progression remains unclear.
methodsIntegrated bioinformatics, including weighted gene co-expression network analysis and machine learning, were applied to the TCGA cohort and validated in an age-stratified clinical cohort. In vitro assays evaluated proliferation, apoptosis, ATP, and Reactive Oxygen Species (ROS) in NRP1-silenced H1299 cells. Mechanisms were investigated using endogenous Co-Immunoprecipitation (Co-IP) and rescue experiments with AGER siRNA and the ROS scavenger N-Acetylcysteine (NAC).
resultsBioinformatics identified AGER as a key NRP1 downstream target. Clinically, NRP1 was significantly upregulated exclusively in elderly (≥65-years) NSCLC patients, whereas AGER was consistently downregulated. Functionally, NRP1 silencing inhibited proliferation, induced G1-phase arrest, and triggered mitochondria-dependent apoptosis characterized by severe ATP depletion and ROS accumulation. Endogenous Co-IP confirmed a direct physical interaction between NRP1 and AGER. Importantly, the oxidative stress and apoptotic phenotypes induced by NRP1 knockdown were effectively reversed by AGER silencing or NAC treatment.
conclusionThe NRP1-AGER-ROS axis critically regulates tumor progression and oxidative stress in NSCLC, particularly in elderly patients, representing a promising age-associated therapeutic target.
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