ReviewCells2019
Targeting the Canonical WNT/β-Catenin Pathway in Cancer Treatment Using Non-Steroidal Anti-Inflammatory Drugs.
Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 91 citations in OpenAlex.
- Inhibition of WNT signaling sensitizes CRC cells to anti-tumor effects of retinoids: basis for new drug combinations in oncology.Cancer biology & therapy · 2026Article
- Hypoxia and aspirin additively increase intracellular glutamine accumulation in PIK3CA-mutated colorectal cancer cells.Scientific reports · 2026Article
- NLRP12 in cancer: a context-dependent regulator of tumor progression, immunity, and metabolism.Frontiers in oncology · 2026Review
- PFOS caused fertility defects and disrupted spermatogenic gene networks in medaka with a transgenerational history of ancestral BPA exposure.Environmental research · 2025Article
- Two-sample Mendelian randomization analysis of the causal association between circulating inflammatory proteins and osteosarcoma.Discover oncology · 2025Article
- Wnt Signaling and Circular RNAs in Esophageal and Gastric Cancers: Opportunities for Early Detection and Targeted Therapy.Journal of clinical medicine · 2025Review
- Review
- Unraveling the role of heavy metals xenobiotics in cancer: a critical review.Discover oncology · 2024Review
- PPARs in Clinical Experimental Medicine after 35 Years of Worldwide Scientific Investigations and Medical Experiments.Biomolecules · 2024Review
- Advances in molecular mechanisms of inflammatory bowel disease‑associated colorectal cancer (Review).Oncology letters · 2024Review
- β-Sitosterol suppresses hepatocellular carcinoma growth and metastasis via FOXM1-regulated Wnt/β-catenin pathway.Journal of cellular and molecular medicine · 2024Article
- The potential therapeutic role of curcumin in osteoporosis treatment: based on multiple signaling pathways.Frontiers in pharmacology · 2024Review
- Theoretical basis validation and oxidative stress markers for cancer prevention clinical trials of aspirin.Scientific reports · 2023Article
- Cancer-associated inflammation: pathophysiology and clinical significance.Journal of cancer research and clinical oncology · 2023Review
- Construction of an oxidative stress-related lncRNAs signature to predict prognosis and the immune response in gastric cancer.Scientific reports · 2023Article
- A nonsteroidal anti-inflammatory drug, zaltoprofen, inhibits the growth of extraskeletal chondrosarcoma cells by inducing PPARγ, p21, p27, and p53.Cell cycle (Georgetown, Tex.) · 2023Article
- Aspirin Use Is Associated With Improved Outcomes in Inflammatory Breast Cancer Patients.Journal of breast cancer · 2023Article
- Review
- The FDA-Approved Drug Pyrvinium Selectively Targets ERCancers · 2022Article
- A Comprehensive Review on the Anti-Cancer Effects of Oleuropein.Life (Basel, Switzerland) · 2022Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic inflammation and oxidative stress are common and co-substantial pathological processes accompanying and contributing to cancers. Numerous epidemiological studies have indicated that non-steroidal anti-inflammatory drugs (NSAIDs) could have a positive effect on both the prevention of cancer and tumor therapy. Numerous hypotheses have postulated that NSAIDs could slow tumor growth by acting on both chronic inflammation and oxidative stress. This review takes a closer look at these hypotheses. In the cancer process, one of the major signaling pathways involved is the WNT/β-catenin pathway, which appears to be upregulated. This pathway is closely associated with both chronic inflammation and oxidative stress in cancers. The administration of NSAIDs has been observed to help in the downregulation of the WNT/β-catenin pathway and thus in the control of tumor growth. NSAIDs act as PPARγ agonists. The WNT/β-catenin pathway and PPARγ act in opposing manners. PPARγ agonists can promote cell cycle arrest, cell differentiation, and apoptosis, and can reduce inflammation, oxidative stress, proliferation, invasion, and cell migration. In parallel, the dysregulation of circadian rhythms (CRs) contributes to cancer development through the upregulation of the canonical WNT/β-catenin pathway. By stimulating PPARγ expression, NSAIDs can control CRs through the regulation of many key circadian genes. The administration of NSAIDs in cancer treatment would thus appear to be an interesting therapeutic strategy, which acts through their role in regulating WNT/β-catenin pathway and PPARγ activity levels.
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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.