ArticleCell death & disease2022
The anthelmintic drug niclosamide induces GSK-β-mediated β-catenin degradation to potentiate gemcitabine activity, reduce immune evasion ability and suppress pancreatic cancer progression.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.
What it found
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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
23 citing papers in PubMed, 32 citations in OpenAlex.
- Repurposing niclosamide to mitigate inflammaging: a review of multi-target mechanisms in cellular senescence and age-related decline.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Translational potential of safe-by-design nanoengineered niclosamide in viral and cancer therapy.Materials today. Bio · 2025Article
- Repurposing Rafoxanide: From Parasite Killer to Cancer Fighter.Biomedicines · 2025Review
- Wnt/β-catenin mediated signaling pathways in cancer: recent advances, and applications in cancer therapy.Molecular cancer · 2025Review
- Targeting stromal components in pancreatic ductal adenocarcinoma: a review.Ecancermedicalscience · 2025Review
- Niclosamide-Loaded Polyanhydride Nanoparticles to Combat Gemcitabine Resistance in Pancreatic Cancer.Regenerative engineering and translational medicine · 2025Article
- Dorsomorphin Suppresses EMT to Reduce AR-Negative Prostate Cancer Metastasis by Synergistically Antagonizing JAK2/STAT3 and Gli2-Independent Shh Activation.Prostate cancer · 2025Article
- Smad4 regulates TGF-β1-mediated hedgehog activation to promote epithelial-to-mesenchymal transition in pancreatic cancer cells by suppressing Gli1 activity.Computational and structural biotechnology journal · 2024Article
- Ubiquitin modification in the regulation of tumor immunotherapy resistance mechanisms and potential therapeutic targets.Experimental hematology & oncology · 2024Review
- Lymphocyte antigen 6 family member E suppresses apoptosis and promotes pancreatic cancer growth and migration via Wnt/β-catenin pathway activation.Scientific reports · 2024Article
- The crosstalk role of CDKN2A between tumor progression and cuproptosis resistance in colorectal cancer.Aging · 2024Article
- The Antifungal Potential of Niclosamide and Structurally Related Salicylanilides.International journal of molecular sciences · 2024Review
- The pluripotency factor NANOG contributes to mesenchymal plasticity and is predictive for outcome in esophageal adenocarcinoma.Communications medicine · 2024Article
- Chloroxine inhibits pancreatic cancer progression through targeted antagonization of the PI3K/AKT/mTOR signaling pathway.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Article
- Salicylanilides and Their Anticancer Properties.International journal of molecular sciences · 2023Review
- High Throughput FISH Screening Identifies Small Molecules That Modulate Oncogenic lncRNA MALAT1 via GSK3B and hnRNPs.Non-coding RNA · 2023Article
- Niclosamide is a potential candidate for the treatment of chemo-resistant osteosarcoma.Genetics and molecular biology · 2023Article
- Exploiting the molecular subtypes and genetic landscape in pancreatic cancer: the quest to find effective drugs.Frontiers in genetics · 2023Review
- Chebulagic acid suppresses gastric cancer by inhibiting the AURKA/β-catenin/Wnt pathway.Frontiers in pharmacology · 2023Article
- Drug Repurposing to Enhance Antitumor Response to PD-1/PD-L1 Immune Checkpoint Inhibitors.Cancers · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Niclosamide, a cell-permeable salicylanilide, was approved by the Food and Drug Administration for its anthelmintic efficiency. A growing body of evidence in recent years suggests that niclosamide exhibits potential tumor-suppressive activity. However, the role and molecular mechanism of niclosamide in pancreatic cancer remain unclear. In this study, niclosamide inhibited proliferation of pancreatic cancer cells (PCCs), induced apoptosis via the mitochondrial-mediated pathway, and suppressed cell migration and invasion by antagonizing epithelial-to-mesenchymal transition. Also, niclosamide inhibited tumor growth and metastasis in pancreatic cancer xenograft mouse models. Mechanistically, niclosamide exerted these therapeutic effects via targeting β-catenin. Niclosamide did not reduce β-catenin mRNA expression in PCCs, but significantly downregulated its protein level. Moreover, niclosamide induced β-catenin phosphorylation and protein degradation. Interestingly, niclosamide also induced GSK-3β phosphorylation, which is involved in the ubiquitination degradation of β-catenin. Pharmacological activation of β-catenin by methyl vanillate and β-catenin overexpression abolished the inhibitory effects of niclosamide. Furthermore, niclosamide potentiated the antitumor effect of the chemotherapy drug gemcitabine and reduced the ability of cancer immune evasion by downregulating the expression levels of PD-L1, which is involved in T cell immunity. Thus, our study indicated that niclosamide induces GSK-β-mediated β-catenin degradation to potentiate gemcitabine activity, reduce immune evasion ability, and suppress pancreatic cancer progression. Niclosamide may be a potential therapeutic candidate for pancreatic cancer.
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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.