ArticleCancer prevention research (Philadelphia, Pa.)2010
Diallyl trisulfide inhibits activation of signal transducer and activator of transcription 3 in prostate cancer cells in culture and in vivo.
Article in Cancer prevention research (Philadelphia, Pa.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 45 citations in OpenAlex.
- The Anticancer Effects of the Garlic Organosulfide Diallyl Trisulfide through the Attenuation of B[a]P-Induced Oxidative Stress, AhR Expression, and DNA Damage in Human Premalignant Breast Epithelial (MCF-10AT1) Cells.International journal of molecular sciences · 2024Article
- Involvement of adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper 1 in diallyl trisulfide-induced cytotoxicity in hepatocellular carcinoma cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Effect of Diallyl Trisulfide on TNF-α-induced CCL2/MCP-1 Release in Genetically Different Triple-negative Breast Cancer Cells.Anticancer research · 2021Article
- Role of hydrogen sulfide donors in cancer development and progression.International journal of biological sciences · 2021Review
- Diallyl Trisulfide Inhibits Leptin-induced Oncogenic Signaling in Human Breast Cancer Cells but Fails to Prevent Chemically-induced Luminal-type Cancer in Rats.Journal of cancer prevention · 2020Article
- Prostate Cancer Disparity, Chemoprevention, and Treatment by Specific Medicinal Plants.Nutrients · 2019Review
- New sulfurated derivatives of cinnamic acids and rosmaricine as inhibitors of STAT3 and NF-κB transcription factors.Journal of enzyme inhibition and medicinal chemistry · 2017Article
- Dietary Bioactive Diallyl Trisulfide in Cancer Prevention and Treatment.International journal of molecular sciences · 2017Review
- Hyperhomocysteinemia, Suppressed Immunity, and Altered Oxidative Metabolism Caused by Pathogenic Microbes in Atherosclerosis and Dementia.Frontiers in aging neuroscience · 2017Review
- Phytochemicals and PI3K Inhibitors in Cancer-An Insight.Frontiers in pharmacology · 2017Review
- At High Levels, Constitutively Activated STAT3 Induces Apoptosis of Chronic Lymphocytic Leukemia Cells.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Article
- Dietary supplemented 2-mercaptoethanol prevents spontaneous and delays virally-induced murine mammary tumorigenesis.Cancer biology & therapy · 2013Article
- Anticancer activity and chemoprevention of xenobiotic organosulfurs in preclinical model systems.Oncology discovery · 2013Article
- Molecular mechanisms and targets of cancer chemoprevention by garlic-derived bioactive compound diallyl trisulfide.Indian journal of experimental biology · 2011Review
- Garlic constituent diallyl trisulfide suppresses x-linked inhibitor of apoptosis protein in prostate cancer cells in culture and in vivo.Cancer prevention research (Philadelphia, Pa.) · 2011Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Signal transducer and activator of transcription 3 (STAT3) is an oncogenic transcription factor implicated in prostate carcinogenesis. The present study shows that diallyl trisulfide (DATS), a promising cancer-chemopreventive constituent of processed garlic, inhibits phosphorylation of STAT3 in prostate cancer cells in culture and in vivo. Exposure of DU145 and LNCaP human prostate cancer cells to growth-suppressive and pharmacologically relevant concentrations of DATS (20 and 40 μmol/L) resulted in suppression of constitutive (DU145) as well as interleukin-6 (IL-6)-induced (LNCaP) phosphorylation of STAT3 (Tyr(705)), which correlated with inhibition of Janus-activated kinase 2 phosphorylation. Constitutive and/or IL-6-induced nuclear translocation of pSTAT3 and STAT3 dimerization was also markedly inhibited on treatment with DATS in both cell lines. Inhibition of prostate cancer development in transgenic adenocarcinoma of mouse prostate mice by gavage of DATS correlated with a visible decrease in the levels of pSTAT3. Interestingly, the IL-6-mediated activation of STAT3 largely failed to confer protection against proapoptotic response to DATS in both cells. Likewise, DATS-mediated inhibition of cell migration was either not affected or minimally reversed by IL-6 treatment or ectopic expression of constitutively active STAT3. In conclusion, the present study indicates that DATS treatment suppresses STAT3 phosphorylation in prostate cancer cells in culture and in vivo, but activation of this oncogenic transcription factor is largely dispensable for cellular responses to DATS. Ability of DATS to overcome STAT3 activation is a therapeutic advantage for this chemopreventive agent.
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