ArticleBreast cancer research and treatment2014
Diallyl trisulfide inhibits estrogen receptor-α activity in human breast cancer cells.
Article in Breast cancer research and treatment, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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Who cites it
23 citing papers in PubMed, 48 citations in OpenAlex.
- Modulation of Wnt/Beta-Catenin Pathway by Major Dietary Phytochemicals Against Breast Cancer Development.Biology · 2025Review
- The potential role of hydrogen sulfide in cancer cell apoptosis.Cell death discovery · 2024Review
- Article
- Diallyl Trisulfide Induces ROS-Mediated Mitotic Arrest and Apoptosis and Inhibits HNSCC Tumor Growth and Cancer Stemness.Cancers · 2024Article
- The potential of diallyl trisulfide for cancer prevention and treatment, with mechanism insights.Frontiers in cell and developmental biology · 2024Review
- Dietary macrominerals: Updated review of their role and orchestration in human nutrition throughout the life cycle with sex differences.Current research in food science · 2023Review
- Updates on the anticancer potential of garlic organosulfur compounds and their nanoformulations: Plant therapeutics in cancer management.Frontiers in pharmacology · 2023Review
- Monocarboxylate transporter 1 is a novel target for breast cancer stem like-cell inhibition by diallyl trisulfide.Molecular carcinogenesis · 2022Article
- Breast Cancer Selective Disruption of Actin Cytoskeleton by Diallyl Trisulfide.Journal of cancer prevention · 2022Article
- Diallyl disulfide and diallyl trisulfide in garlic as novel therapeutic agents to overcome drug resistance in breast cancer.Journal of pharmaceutical analysis · 2022Review
- Gene Expression Changes by Diallyl Trisulfide Administration in Chemically-induced Mammary Tumors in Rats.Journal of cancer prevention · 2022Article
- Contribution of Nanoscience Research in Antioxidants Delivery Used in Nutricosmetic Sector.Antioxidants (Basel, Switzerland) · 2022Review
- Mechanistic Targets of Diallyl Trisulfide in Human Breast Cancer Cells Identified by RNA-seq Analysis.Journal of cancer prevention · 2021Article
- Diet, Sports, and Psychological Stress as Modulators of Breast Cancer Risk: Focus onFrontiers in nutrition · 2021Article
- Health Benefits of Plant-Derived Sulfur Compounds, Glucosinolates, and Organosulfur Compounds.Molecules (Basel, Switzerland) · 2020Review
- 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
- Prolyl isomerase Pin1: a promoter of cancer and a target for therapy.Cell death & disease · 2018Review
- A possible mechanism of inhibition of U87MG and SH-SY5Y cancer cell proliferation by diallyl trisulfide and other aspects of its activity.Amino acids · 2017Article
- Dietary Bioactive Diallyl Trisulfide in Cancer Prevention and Treatment.International journal of molecular sciences · 2017Review
- Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Organosulfur compounds from garlic effectively inhibit growth of transplanted as well as spontaneous cancers in preclinical animal models without any adverse side effects. However, the mechanisms underlying anticancer effect of this class of compounds are not fully understood. This study reports, for the first time, that garlic organosulfide diallyl trisulfide (DATS) inhibits estrogen receptor-α (ER-α) activity in human breast cancer cells. Exposure of MCF-7 and T47D cells to DATS resulted in downregulation of ER-α protein, which peaked between 12- and 24-h post-treatment. DATS was relatively more effective in suppressing ER-α protein expression compared with its mono and disulfide analogs. The 17β-estradiol (E2)-induced expression of pS2 and cyclin D1, ER-α target gene products, was also decreased in the presence of DATS. Downregulation of ER-α protein expression resulting from DATS treatment was accompanied by a decrease in nuclear levels of ER-α protein, ER-α mRNA suppression, and inhibition of ERE2e1b-luciferase reporter activity. DATS-mediated inhibition of cell viability and apoptosis induction were not affected in the presence of E2. In agreement with these results, ectopic expression of ER-α in MDA-MB-231 cell line failed to confer any protection against cell proliferation inhibition or apoptosis induction resulting from DATS exposure. DATS treatment caused a decrease in protein levels of peptidyl-prolyl cis-trans isomerase (Pin1), and overexpression of Pin1 partially attenuated ER-α downregulation by DATS. DATS-induced apoptosis was modestly but significantly augmented by overexpression of Pin1. In conclusion, this study identifies ER-α as a novel target of DATS in mammary cancer cells.
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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.