ArticleAnnals of translational medicine2021
Apurinic/apyrimidinic endonuclease 1/reduction-oxidation effector factor-1 (APE1) regulates the expression of NLR family pyrin domain containing 3 (NLRP3) inflammasome through modulating transcription factor NF-κB and promoting the secretion of inflammatory mediators in macrophages.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Electroacupuncture Stimulation of the Head Motor Area Alleviates Brain Cell Pyroptosis and Neurobehaviors in Stroke Rats Through the NF-κB/NLRP3 Signaling Axis.Neurochemical research · 2026Article
- NRF2 Antioxidant Response and Interferon-Stimulated Genes Are Differentially Expressed in SARS-CoV-2-Positive Young Subjects.Immunity, inflammation and disease · 2025Article
- Targeting APE1/Ref-1 to alleviate formalin-induced pain and spinal neuro-inflammation in rats: a promising therapeutic approach.Frontiers in neuroscience · 2025Article
- The APE1/REF-1 and the hallmarks of cancer.Molecular biology reports · 2024Review
- APEX1 Nuclease and Redox Functions are Both Essential for Adult Mouse Hematopoietic Stem and Progenitor Cells.Stem cell reviews and reports · 2023Article
- Marine Compounds, Mitochondria, and Malignancy: A Therapeutic Nexus.Marine drugs · 2022Review
- Exploring the Mechanism of Ling-Gui-Zhu-Gan Decoction in Ventricular Remodeling after Acute Myocardial Infarction Based on UPLC andEvidence-based complementary and alternative medicine : eCAM · 2022Article
- APE1/Ref-1 - One Target with Multiple Indications: Emerging Aspects and New Directions.Journal of cellular signaling · 2021Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammatory mediators play an important role in the occurrence, development, and metastasis of tumors. The aim of the present study was to elucidate the effect of apurinic/apyrimidinic endonuclease 1/reduction-oxidation effector factor-1 (APE1) on inflammatory mediator secretion, which is dependent on the APE1-mediated NLR family pyrin domain containing 3 (NLRP3) regulatory mechanism.
methodsThe human myeloid leukemia mononuclear cell line (THP-1) cells were cultured and polarized to M2 subset macrophages. Enzyme-linked immunosorbent assay was used for determining tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-18, IL-10, and IL-33 levels. Reverse transcription-polymerase chain reaction and western blot were used for evaluating TNF-α, NLR family pyrin domain containing 1 (NLRP1), NLRP3, caspase-1, and apoptosis-associated speck-like protein containing a card expression. Plasmid silencing
resultsAPE1 significantly induced LPS-induced pro-inflammatory cytokine production, including TNF-α, IL-1β, and IL18, compared with THP-1 cells without APE1 treatment (P<0.05). APE1 promoted LPS-induced NLRP3 inflammasome activation by modulating the gene transcription of NLRP3-associated molecules. APE1 enhanced LPS-induced NLRP3 inflammasome activation by regulating NLRP3 and caspase-1 protein expression. APE1 improved NLRP3 activity by modulating the interaction between NLRP3 and NF-κB, and the modulation of NF-κB. APE1 promoted LPS-induced NLRP3 inflammasome activation through an NF-κB-dependent pathway.
conclusionsAPE1 regulates the expression of NLRP3 by modulating transcription factor NF-κB and further promoting the secretion of inflammatory mediators IL-1β and IL-18 in macrophages. The findings of the present study provide theoretical and experimental bases for the design of tumor-associated macrophage (TAM)-targeted therapy, with APE1 as the target molecule.
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