ArticleJournal of the National Cancer Institute2009
The role of STAT-3 in the induction of apoptosis in pancreatic cancer cells by benzyl isothiocyanate.
Article in Journal of the National Cancer Institute, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
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Who cites it
81 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.
- Cruciferous vegetable consumption and the risk of pancreatic cancer: a meta-analysis.World journal of surgical oncology · 2015Pooled it
- CNOT2 /c-Myc/STAT3 signaling is critically involved in glycolysis mediated apoptosis of benzyl isothiocyanate in hepatocellular carcinoma.Scientific reports · 2026Article
- Glucosinolates in cancer prevention and treatment: experimental and clinical evidence.Medical oncology (Northwood, London, England) · 2023Review
- The role and mechanism of JAK2/STAT3 signaling pathway regulated by m6A methyltransferase KIAA1429 in osteosarcoma.Journal of bone oncology · 2023Article
- Inflammatory Cytokines and Radiotherapy in Pancreatic Ductal Adenocarcinoma.Biomedicines · 2022Review
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- Assessment of Methodological Pipelines for the Determination of Isothiocyanates Derived from Natural Sources.Antioxidants (Basel, Switzerland) · 2022Review
- Comprehensive analysis of the prognostic and immunotherapeutic implications of STAT family members in human colorectal cancer.Frontiers in genetics · 2022Article
- Benzyl Isothiocyanate, a Vegetable-Derived Compound, Induces Apoptosis via ROS Accumulation and DNA Damage in Canine Lymphoma and Leukemia Cells.International journal of molecular sciences · 2021Article
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- Role of hydrogen sulfide donors in cancer development and progression.International journal of biological sciences · 2021Review
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- Polyphenols as Possible Agents for Pancreatic Diseases.Antioxidants (Basel, Switzerland) · 2020Review
- Isocorydine decrease gemcitabine-resistance by inhibiting epithelial-mesenchymal transition via STAT3 in pancreatic cancer cells.American journal of translational research · 2020Article
- Bioactive Compounds: Multi-Targeting Silver Bullets for Preventing and Treating Breast Cancer.Cancers · 2019Review
- Role of Phytochemicals in Cancer Prevention.International journal of molecular sciences · 2019Review
- Atovaquone: An Antiprotozoal Drug Suppresses Primary and Resistant Breast Tumor Growth by Inhibiting HER2/β-Catenin Signaling.Molecular cancer therapeutics · 2019Article
- The Role of Isothiocyanates as Cancer Chemo-Preventive, Chemo-Therapeutic and Anti-Melanoma Agents.Antioxidants (Basel, Switzerland) · 2019Review
- HER2-mediated GLI2 stabilization promotes anoikis resistance and metastasis of breast cancer cells.Cancer letters · 2019Article
21 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundBenzyl isothiocyanate (BITC), a compound found in cruciferous vegetables, has been reported to have anticancer properties, but the mechanism whereby it inhibits growth of human pancreatic cancer cells is incompletely understood.
methodsHuman pancreatic cancer cells (BxPC-3, AsPC-1, Capan-2, MiaPaCa-2, and Panc-1) and immortalized human pancreatic cells (HPDE-6) were treated with vehicle or with BITC at 5-40 microM, cell survival was evaluated by sulforhodamine B assay, and apoptosis by caspase-3 and poly-ADP ribose polymerase cleavage or by a commercial assay for cell death. Total and activated signal transducer and activator of transcription-3 (STAT-3) protein expression in the cells were examined by western blotting, STAT-3 mRNA levels by reverse transcription-polymerase chain reaction, and STAT-3 DNA-binding and transcriptional activity by commercially available binding and reporter assays. The effects of BITC treatment on tumor growth, apoptosis, and STAT-3 protein expression in vivo were studied in xenografts of BxPC-3 pancreatic tumor cells in athymic nude mice. All statistical tests were two-sided.
resultsBITC treatment reduced cell survival and induced apoptosis in BxPC-3, AsPC-1, Capan-2, and MiaPaCa-2 cells, and to a much lesser extent in Panc-1 cells, but not in HPDE-6 cells. It also reduced levels of activated and total STAT-3 protein, and as a result, STAT-3 DNA-binding and transcriptional activities. Overexpression of STAT-3 in BxPC-3 cells inhibited BITC-induced apoptosis and restored STAT-3 activity. In mice that were fed BITC (60 micromol/wk, five mice, 10 tumors per group), growth of BxPC-3 pancreatic tumor xenografts was suppressed compared with control mice (at 6 weeks, mean tumor volume of control vs BITC-treated mice = 334 vs 172 mm3, difference =162 mm3, 95% confidence interval = 118 to 204 mm3; P = .008) and tumors had increased apoptosis and reduced STAT-3 protein expression.
conclusionBITC induces apoptosis in some types of pancreatic cancer cells by inhibiting the STAT-3 signaling pathway.
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