ArticleOncotarget2016
Hypoxia primes human normal prostate epithelial cells and cancer cell lines for the NLRP3 and AIM2 inflammasome activation.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 44 citations in OpenAlex.
- Insights Into Infections and Inflammation in Prostate Cancer Development and Management: An Overview.BioMed research international · 2026Review
- Role of the AIM2 Inflammasome in Cancer: Potential Therapeutic Strategies.Biomedicines · 2025Review
- The Role of AIM2 in Cancer Development: Inflammasomes and Beyond.Journal of Cancer · 2025Review
- Therapeutic Significance of NLRP3 Inflammasome in Cancer: Friend or Foe?International journal of molecular sciences · 2024Review
- Article
- Exploring the role of the inflammasomes on prostate cancer: Interplay with obesity.Reviews in endocrine & metabolic disorders · 2023Review
- NLRP3 and cancer: Pathogenesis and therapeutic opportunities.Pharmacology & therapeutics · 2023Review
- Kicking sleepers out of bed: Macrophages promote reactivation of dormant Cryptococcus neoformans by extracellular vesicle release and non-lytic exocytosis.PLoS pathogens · 2023Article
- NOD-like Receptors-Emerging Links to Obesity and Associated Morbidities.International journal of molecular sciences · 2023Review
- NLRP3 inflammasome in neurodegenerative disease.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Review
- NLRP3 inflammasome promoted the malignant progression of prostate cancer via the activation of caspase-1.Cell death discovery · 2021Article
- Qianliexin capsule exerts anti-inflammatory activity in chronic non-bacterial prostatitis and benign prostatic hyperplasia via NF-κB and inflammasome.Journal of cellular and molecular medicine · 2021Article
- Mechanisms of NLRP3 priming in inflammaging and age related diseases.Cytokine & growth factor reviews · 2020Review
- Beneficial Effects of Inflammatory Cytokine-Targeting Aptamers in an Animal Model of Chronic Prostatitis.International journal of molecular sciences · 2020Article
- Role of the NLRP3 Inflammasome: Insights Into Cancer Hallmarks.Frontiers in immunology · 2020Review
- NLRP3 Inflammasome From Bench to Bedside: New Perspectives for Triple Negative Breast Cancer.Frontiers in oncology · 2020Review
- NLRP3 Inflammasome Activation in Cancer: A Double-Edged Sword.Frontiers in immunology · 2020Review
- Role of the NLRP3 inflammasome in cancer.Molecular cancer · 2018Review
- HIV vaccine candidate activation of hypoxia and the inflammasome in CD14Nature medicine · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The molecular mechanisms by which hypoxia contributes to prostatic chronic inflammation (PCI) remain largely unknown. Because hypoxia stimulates the transcriptional activity of NF-κB, which "primes" cells for inflammasome activation by inducing the expression of NLRP3 or AIM2 receptor and pro-IL-1β, we investigated whether hypoxia could activate the NLRP3 and AIM2 inflammasome in human normal prostate epithelial cells (PrECs) and cancer cell lines. Here we report that hypoxia (1% O2) treatment of PrECs, prostate cell lines, and a macrophage cell line (THP-1) increased the levels of NLRP3, AIM2, and pro-IL-1β. Further, hypoxia in cells potentiated activation of the NLRP3 and AIM2 inflammasome activity. Notably, hypoxia "primed" cells for NLRP3 and AIM2 inflammasome activation through stimulation of the NF-κB activity. Our observations support the idea that hypoxia in human prostatic tumors contributes to PCI, in part, by priming cells for the activation of NLRP3 and AIM2 inflammasome.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.