ArticleOncoTargets and therapy2019
The anthelmintic drug flubendazole induces cell apoptosis and inhibits NF-κB signaling in esophageal squamous cell carcinoma.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Effects of nanoflubendazole and purinergic signaling modulation in overcoming neuroblastoma chemoresistance.Purinergic signalling · 2025Article
- Anticancer role of flubendazole: Effects and molecular mechanisms (Review).Oncology letters · 2024Review
- Rafoxanide negatively modulates STAT3 and NF-κB activity and inflammation-associated colon tumorigenesis.Cancer science · 2024Article
- Immune Checkpoint Inhibitors, Small-Molecule Immunotherapies and the Emerging Role of Neutrophil Extracellular Traps in Therapeutic Strategies for Head and Neck Cancer.International journal of molecular sciences · 2023Review
- Anthelmintic Drugs as Emerging Immune Modulators in Cancer.International journal of molecular sciences · 2023Review
- Transcriptome‑based drug repositioning identifies TPCA‑1 as a potential selective inhibitor of esophagus squamous carcinoma cell viability.International journal of molecular medicine · 2022Article
- Flubendazole Plays an Important Anti-Tumor Role in Different Types of Cancers.International journal of molecular sciences · 2022Review
- Ellagic acid induces esophageal squamous cell carcinoma cell apoptosis by modulating SHP-1/STAT3 signaling.The Kaohsiung journal of medical sciences · 2020Article
- Albendazole-Induced SIRT3 Upregulation Protects Human Leukemia K562 Cells from the Cytotoxicity of MCL1 Suppression.International journal of molecular sciences · 2020Article
- [Flubendazole Inhibits the Proliferation of A549 and H460 Cells and Promotes Autophagy].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2020Article
- Flubendazole elicits anti-cancer effects via targeting EVA1A-modulated autophagy and apoptosis in Triple-negative Breast Cancer.Theranostics · 2020Article
- Ubiquitin-specific protease 44 inhibits cell growth by suppressing AKT signaling in non-small cell lung cancer.The Kaohsiung journal of medical sciences · 2019Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesThe nuclear factor kappa B (NF-κB) signaling is activated in esophageal squamous cell carcinoma (ESCC) and can be used as a potential target for anti-ESCC drug discovery. In this study, we aimed to investigate the function of flubendazole as a novel NF-κB inhibitor in ESCC cells. MATERIALS AND
methodsCell Counting Kit-8 assay was carried out to assess cell viability of ESCC cells. Flow cytometry and immunoblotting were performed to examine cell apoptosis. Immunoblotting assay was used to analyze the protein expression of NF-κB signaling. Luciferase assay was performed to explore the activation of NF-κB. Plasmids were transfected into ESCC cells using Lipofectamine
resultsIn this study, the anthelmintic drug flubendazole was found to inhibit the activation of IκBα kinases (IKKs), block the activation of IκBα, and decrease the phosphorylation of NF-κB p65, which could be a novel NF-κB inhibitor in ESCC cells. We also found that flubendazole inhibited the cell survival of different ESCC cells and induced cell apoptosis in both EC9706 and TE1 cells. Moreover, overexpression of constitutively activated IKKβ markedly decreased the cytotoxic effect of flubendazole on EC9706 and TE1 cells. In addition, flubendazole also showed a synergistic effect on ESCC cells when combined with doxorubicin.
conclusionThe results above demonstrated that flubendazole showed its anti-tumor action by suppressing the NF-κB signaling pathway and suggested that flubendazole might be re-purposed for anti-ESCC therapy in clinic as a single agent or in combination with other anti-tumor drugs.
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