ArticleThe Journal of international medical research2021
Diallyl trisulfide inhibited tobacco smoke-mediated bladder EMT and cancer stem cell marker expression via the NF-κB pathway
Article in The Journal of international medical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 10 citations in OpenAlex.
- Exosomal circ55033 promotes cigarette smoke-induced bladder cancer by modulating EMT and stem cell properties.Medical oncology (Northwood, London, England) · 2026Article
- Hypoxia-induced HIF-1α/VASN promotes bladder cancer progression.Scientific reports · 2025Article
- Diallyl Trisulfide Enhances Doxorubicin Chemosensitivity by Inhibiting the Warburg Effect and Inducing Apoptosis in Breast Cancer Cells.Journal of Cancer · 2025Article
- Skullcapflavone II suppresses TGF-β-induced corneal epithelial mesenchymal transitionInternational journal of ophthalmology · 2025Article
- Decoding Oral Carcinogenesis and Tumor Progression in Whole Cigarette Smoke Exposure: A Systematic Review.Cureus · 2024Review
- Diallyl trisulfide inhibits osteosarcoma 143B cell migration, invasion and EMT by inducing autophagy.Heliyon · 2024Article
- The potential of diallyl trisulfide for cancer prevention and treatment, with mechanism insights.Frontiers in cell and developmental biology · 2024Review
- Pesticides and Bladder Cancer: Mechanisms Leading to Anti-Cancer Drug Chemoresistance and New Chemosensitization Strategies.International journal of molecular sciences · 2023Review
- Palmitic Acid Promotes Lung Metastasis of Melanomas via the TLR4/TRIF-Peli1-pNF-κB Pathway.Metabolites · 2022Article
- Global Trends in Research of Treatment on Bladder Cancer with Chinese Medicine Monomer from 2000 to 2021: A Bibliometric Analysis.Journal of oncology · 2022Article
- Targeting Cancer Stem Cells by Dietary Agents: An Important Therapeutic Strategy against Human Malignancies.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study examined the effect of the NF-κB pathway on tobacco smoke-elicited bladder epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) marker expression
methodsBALB/c mice were exposed to tobacco smoke and treated with an NF-κB inhibitor and DATS. Western blotting, quantitative real-time PCR, and immunohistochemical staining were used to detect the changes of relevant indices.
resultsPhosphorylated inhibitor of kappa-B kinase alpha/beta expression and p65 and p50 nuclear transcription were increased by tobacco smoke exposure, whereas inhibitor of kappa-B expression was decreased. In addition, tobacco smoke reduced the expression of epithelial markers but increased that of mesenchymal and CSC markers. Our study further demonstrated that tobacco smoke-mediated EMT and CSC marker expression were attenuated by inhibition of the NF-κB pathway. Moreover, DATS reversed tobacco smoke-induced NF-κB pathway activation, EMT, and the acquisition of CSC properties in bladder tissues.
conclusionsThese data suggested that the NF-κB pathway regulated tobacco smoke-induced bladder EMT, CSC marker expression, and the protective effects of DATS.
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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.