What is the clinical evidence from this study?

Study design: Other. Population: Non-Small Cell Lung Cancer (NSCLC). Intervention: NRP1 silencing. Primary outcome: proliferation, apoptosis, ATP, and Reactive Oxygen Species (ROS).

What question did this study set out to answer?

To elucidate the functional role of Neuropilin-1 (NRP1) and its mechanistic connection to oxidative stress and AGER signaling in non-small cell lung cancer (NSCLC) progression.

August 14, 2026

NRP1 silencing induces ROS-mediated cell cycle arrest and mitochondrial apoptosis in non-small cell lung cancer via upregulation of AGER.

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Key result

NRP1 silencing inhibits proliferation and triggers apoptosis in non-small cell lung cancer via AGER upregulation.

Why the study?

The specific role of Neuropilin-1 (NRP1) and its link to oxidative stress in Non-Small Cell Lung Cancer progression remained unclear.

Population

TCGA cohort, an age-stratified clinical cohort, and H1299 cells

Comparison

NRP1 silencing vs controls and rescue experiments

Design

Integrated bioinformatics, clinical validation, and in vitro experimental study

Authors

YYYa YangXuzhou Medical College YLYing LiXuzhou Medical College YZYongjuan ZhaoXuzhou Medical College

Discussion

Member takes

Implication

NRP1 inhibition merits preclinical exploration in NSCLC; leaves open clinical translation and patient outcomes.

Key Points

To elucidate the functional role of Neuropilin-1 (NRP1) and its mechanistic connection to oxidative stress and AGER signaling in non-small cell lung cancer (NSCLC) progression.
Analyzed TCGA datasets using weighted gene co-expression network analysis (WGCNA) and machine learning, validating expression in an age-stratified NSCLC clinical cohort.
Conducted in vitro assays in NRP1-silenced H1299 lung cancer cells to evaluate cell proliferation, cell cycle distribution, apoptosis, ROS production, and ATP levels.
Investigated physical and functional interactions using endogenous co-immunoprecipitation and rescue experiments with AGER siRNA and the ROS scavenger N-acetylcysteine.
Bioinformatic and clinical analyses revealed NRP1 is significantly upregulated specifically in elderly patients (≥65 years), whereas its downstream partner AGER is downregulated.
NRP1 knockdown induced G1-phase arrest, ATP depletion, ROS accumulation, and mitochondria-dependent apoptosis through direct physical interaction with AGER.
The oxidative stress and apoptotic responses provoked by NRP1 silencing were reversed by AGER co-silencing or antioxidant treatment with N-acetylcysteine.

Structured PICO

Population

TCGA cohort, age-stratified clinical cohort of Non-Small Cell Lung Cancer (NSCLC) patients, and in vitro H1299 cells

Intervention

NRP1 silencing (knockdown)

Comparator

Control, AGER siRNA, and ROS scavenger N-Acetylcysteine (NAC) rescue experiments

Outcome

Proliferation, apoptosis, ATP, and Reactive Oxygen Species (ROS) levelssurrogate

The NRP1-AGER-ROS axis regulates tumor progression and oxidative stress in NSCLC, particularly in elderly patients, suggesting a potential therapeutic target.

Cite This Study

Yang et al. (2026) studied Non-Small Cell Lung Cancer (NSCLC). NRP1 silencing was evaluated on proliferation, apoptosis, ATP, and Reactive Oxygen Species (ROS). NRP1 silencing inhibited proliferation, induced G1-phase arrest, and triggered mitochondria-dependent apoptosis in non-small cell lung cancer cells via upregulation of AGER.

synapsesocial.com/papers/6a7ee587b70b84ec8b91480b https://doi.org/10.1016/j.clinsp.2026.101080

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August 14, 2026

NRP1 silencing induces ROS-mediated cell cycle arrest and mitochondrial apoptosis in non-small cell lung cancer via upregulation of AGER.

View Full Paper

Ask AI

Bookmark

Key result

NRP1 silencing inhibits proliferation and triggers apoptosis in non-small cell lung cancer via AGER upregulation.

Why the study?

The specific role of Neuropilin-1 (NRP1) and its link to oxidative stress in Non-Small Cell Lung Cancer progression remained unclear.

Population

TCGA cohort, an age-stratified clinical cohort, and H1299 cells

Comparison

NRP1 silencing vs controls and rescue experiments

Design

Integrated bioinformatics, clinical validation, and in vitro experimental study

Authors

YYYa YangXuzhou Medical College YLYing LiXuzhou Medical College YZYongjuan ZhaoXuzhou Medical College

Discussion

Member takes

Implication

NRP1 inhibition merits preclinical exploration in NSCLC; leaves open clinical translation and patient outcomes.

Key Points

To elucidate the functional role of Neuropilin-1 (NRP1) and its mechanistic connection to oxidative stress and AGER signaling in non-small cell lung cancer (NSCLC) progression.
Analyzed TCGA datasets using weighted gene co-expression network analysis (WGCNA) and machine learning, validating expression in an age-stratified NSCLC clinical cohort.
Conducted in vitro assays in NRP1-silenced H1299 lung cancer cells to evaluate cell proliferation, cell cycle distribution, apoptosis, ROS production, and ATP levels.
Investigated physical and functional interactions using endogenous co-immunoprecipitation and rescue experiments with AGER siRNA and the ROS scavenger N-acetylcysteine.
Bioinformatic and clinical analyses revealed NRP1 is significantly upregulated specifically in elderly patients (≥65 years), whereas its downstream partner AGER is downregulated.
NRP1 knockdown induced G1-phase arrest, ATP depletion, ROS accumulation, and mitochondria-dependent apoptosis through direct physical interaction with AGER.
The oxidative stress and apoptotic responses provoked by NRP1 silencing were reversed by AGER co-silencing or antioxidant treatment with N-acetylcysteine.

Structured PICO

Population

TCGA cohort, age-stratified clinical cohort of Non-Small Cell Lung Cancer (NSCLC) patients, and in vitro H1299 cells

Intervention

NRP1 silencing (knockdown)

Comparator

Control, AGER siRNA, and ROS scavenger N-Acetylcysteine (NAC) rescue experiments

Outcome

Proliferation, apoptosis, ATP, and Reactive Oxygen Species (ROS) levelssurrogate

The NRP1-AGER-ROS axis regulates tumor progression and oxidative stress in NSCLC, particularly in elderly patients, suggesting a potential therapeutic target.

Cite This Study

synapsesocial.com/papers/6a7ee587b70b84ec8b91480b https://doi.org/10.1016/j.clinsp.2026.101080

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