ArticleFrontiers in oncology2020
Caffeic Acid Phenethyl Ester Prevents Colitis-Associated Cancer by Inhibiting NLRP3 Inflammasome.
Article in Frontiers in oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.
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Who cites it
24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.
- The Pro-tumor and Anti-tumor Effects of NLRP3 Inflammasome as a New Therapeutic Option for Colon Cancer: a Meta-analysis of Pre-clinical Studies.Journal of gastrointestinal cancer · 2023Pooled it
- The Multifaceted Role and Regulation of Nlrp3 Inflammasome in Colitis-Associated Colo-Rectal Cancer: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Review
- Anwei decoction alleviates chronic atrophic gastritis by modulating the gut microbiota-metabolite axis andWorld journal of gastroenterology · 2026Article
- The emerging role of honeysuckle flower in inflammatory bowel disease.Frontiers in nutrition · 2025Review
- Inflammasomes in Intestinal Disease: Mechanisms of Activation and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- The regulation of pyroptosis by post-translational modifications: molecular mechanisms and therapeutic targets.EBioMedicine · 2024Review
- Article
- The roles of ubiquitination and deubiquitination of NLRP3 inflammasome in inflammation-related diseases: A review.Biomolecules & biomedicine · 2024Review
- Harnessing the Anti-Inflammatory Properties of Polyphenols in the Treatment of Inflammatory Bowel Disease.International journal of biological sciences · 2024Review
- NOD-like Receptor Signaling Pathway in Gastrointestinal Inflammatory Diseases and Cancers.International journal of molecular sciences · 2023Review
- Divergent functions of NLRP3 inflammasomes in cancer: a review.Cell communication and signaling : CCS · 2023Review
- Regulatory mechanisms and therapeutic potential of JAB1 in neurological development and disorders.Molecular medicine (Cambridge, Mass.) · 2023Review
- Therapeutic effects of natural polyphenols on colorectal adenomas: Focus on preclinical studies (Review).Oncology reports · 2023Review
- The Role of Post-Translational Modifications in Regulation of NLRP3 Inflammasome Activation.International journal of molecular sciences · 2023Review
- Neutrophil Extracellular Traps Induce Alveolar Macrophage Pyroptosis by Regulating NLRP3 Deubiquitination, Aggravating the Development of Septic Lung Injury.Journal of inflammation research · 2023Article
- Caffeic acid phenethyl ester attenuates osteoarthritis progression by activating NRF2/HO‑1 and inhibiting the NF‑κB signaling pathway.International journal of molecular medicine · 2022Article
- Cuproptosis related genes associated with Jab1 shapes tumor microenvironment and pharmacological profile in nasopharyngeal carcinoma.Frontiers in immunology · 2022Article
- Pineapple Leaf Phenols Attenuate DSS-Induced Colitis in Mice and Inhibit Inflammatory Damage by Targeting the NF-κB Pathway.Molecules (Basel, Switzerland) · 2021Article
- NLRP3 Ubiquitination-A New Approach to Target NLRP3 Inflammasome Activation.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-lasting inflammation in the intestinal tract renders individuals susceptible to colitis-associated cancer (CAC). The NOD-like receptor protein 3 (NLRP3) inflammasome plays a key role in the progression of inflammatory bowel disease and CAC. Therefore, identifying effective drugs that prevent CAC by targeting NLRP3 inflammasome is of great interest. Here, we aimed to evaluate the anti-inflammatory effect of caffeic acid phenethyl ester (CAPE) on bone marrow-derived macrophages (BMDMs), THP-1 cells, and azoxymethane/dextran sulfate sodium (AOM/DSS)-induced colon cancer mouse model. We also investigated the anti-tumor mechanism of CAPE. We found that CAPE decreased NLRP3 inflammasome activation in BMDMs and THP-1 cells and protected mice from colorectal cancer induced by AOM/DSS. CAPE regulated NLRP3 at the post-transcriptional level by inhibiting reactive oxygen species (ROS) production. However, CAPE did not affect NLRP3 or IL-1β transcription, but instead enhanced NLRP3 binding to ubiquitin molecules, promoting NLRP3 ubiquitination, and contributing to the anti-tumor effect in the AOM/DSS mouse model. Moreover, CAPE suppressed the interaction between NLRP3 and CSN5 but enhanced that between NLRP3 and Cullin1 both
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