What question did this study set out to answer?

To examine whether apigenin mitigates cellular injury and pyroptosis-associated signaling in lung adenocarcinoma cells and identify potential underlying molecular targets.

August 29, 2026Thoracic CancerOpen Access

Apigenin Alleviates Pyroptosis in Lung Adenocarcinoma Cells by Modulating TNF ‐α/ NF ‐ κB Signaling and AIM2 Inflammasome Activation

Q: What does this research mean for the field?

Apigenin alleviates cellular injury and pyroptosis in lung adenocarcinoma cells, potentially by modulating TNF-α/NF-κB signaling and AIM2 inflammasome activation. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

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Authors

KZKairui ZhuYantaishan Hospital YMYulong MuWannan Medical College ZSZhenguo SuSecond Hospital of Shandong University

Discussion

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Implication

In vitro and bioinformatic study demonstrates apigenin reduces pyroptotic injury in lung adenocarcinoma cells, indicating potential therapeutic value targeting inflammatory cell death pathways.

Key Points

To examine whether apigenin mitigates cellular injury and pyroptosis-associated signaling in lung adenocarcinoma cells and identify potential underlying molecular targets.
Treated an in vitro cellular injury model of A549 lung adenocarcinoma cells with apigenin and evaluated cell morphology, viability via CCK-8 assays, and pyroptosis markers.
Applied network pharmacology, molecular docking, and molecular dynamics simulations to predict candidate drug targets.
Analyzed TCGA and GEO datasets to identify pyroptosis-related lung adenocarcinoma subtypes and construct a validated prognostic risk signature.
Apigenin partially restored cell viability, alleviated morphological damage, and decreased levels of GSDMD-N, caspase-1, IL-1β, AIM2, ASC, and TNF-α/NF-κB pathway proteins.
Computational simulations prioritized TNF and AIM2 as primary targets and predicted a stable interaction between apigenin and TNF.
Bioinformatic analyses established a pyroptosis-related gene signature that successfully stratified patient survival in both training and external validation cohorts.

Cite This Study

Zhu et al. (2026) studied this question.

synapsesocial.com/papers/6a92997e8e5d7d1fc0c118bf https://doi.org/10.1111/1759-7714.70383

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August 29, 2026Thoracic CancerOpen Access

Apigenin Alleviates Pyroptosis in Lung Adenocarcinoma Cells by Modulating TNF ‐α/ NF ‐ κB Signaling and AIM2 Inflammasome Activation

View Full Paper

Ask AI

Bookmark

Authors

KZKairui ZhuYantaishan Hospital YMYulong MuWannan Medical College ZSZhenguo SuSecond Hospital of Shandong University

Discussion

Member takes

Implication

In vitro and bioinformatic study demonstrates apigenin reduces pyroptotic injury in lung adenocarcinoma cells, indicating potential therapeutic value targeting inflammatory cell death pathways.

Key Points

To examine whether apigenin mitigates cellular injury and pyroptosis-associated signaling in lung adenocarcinoma cells and identify potential underlying molecular targets.
Treated an in vitro cellular injury model of A549 lung adenocarcinoma cells with apigenin and evaluated cell morphology, viability via CCK-8 assays, and pyroptosis markers.
Applied network pharmacology, molecular docking, and molecular dynamics simulations to predict candidate drug targets.
Analyzed TCGA and GEO datasets to identify pyroptosis-related lung adenocarcinoma subtypes and construct a validated prognostic risk signature.
Apigenin partially restored cell viability, alleviated morphological damage, and decreased levels of GSDMD-N, caspase-1, IL-1β, AIM2, ASC, and TNF-α/NF-κB pathway proteins.
Computational simulations prioritized TNF and AIM2 as primary targets and predicted a stable interaction between apigenin and TNF.
Bioinformatic analyses established a pyroptosis-related gene signature that successfully stratified patient survival in both training and external validation cohorts.

Cite This Study

Zhu et al. (2026) studied this question.

synapsesocial.com/papers/6a92997e8e5d7d1fc0c118bf https://doi.org/10.1111/1759-7714.70383

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