ArticleBiochemical pharmacology2020
The putative endogenous AHR ligand ITE reduces JAG1 and associated NOTCH1 signaling in triple negative breast cancer cells.
Article in Biochemical pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Unraveling the Mechanisms of AhR-Notch Interplay in Mediating Arsenic Trioxide Cytotoxicity in MCF-7 and MDA-MB-231 Breast Cancer Cell Lines.Biological trace element research · 2025Article
- Application of Gene Editing Technology Based on Targeted Delivery Materials in TNBC.ACS omega · 2025Review
- The involvement of exosomes in the tumorigenicity of breast cancer cell lines through the crosstalk between STAT3, Notch, and Wnt signaling pathways.Discover oncology · 2025Article
- Reduced JAG1 Expression Through miR-200 Overexpression or Crispr-Cas Mediated Knockout Impairs TNBC Growth and Metastasis.Molecular carcinogenesis · 2025Article
- RFX5 promotes the progression of triple-negative breast cancer through transcriptional activation of JAG1.Human cell · 2025Article
- High BMI Is Associated with Changes in Peritumor Breast Adipose Tissue That Increase the Invasive Activity of Triple-Negative Breast Cancer Cells.International journal of molecular sciences · 2024Article
- Patterns of immune evasion in triple-negative breast cancer and new potential therapeutic targets: a review.Frontiers in immunology · 2024Review
- Aryl hydrocarbon receptor: An emerging player in breast cancer pathogenesis and its potential as a drug target (Review).Molecular medicine reports · 2024Review
- The potential of aryl hydrocarbon receptor as receptors for metabolic changes in tumors.Frontiers in oncology · 2024Review
- Review
- Article
- Nuclear Transporting Factor 2 as a Novel Biomarker of Head and Neck Squamous Cell Carcinoma and Associated with T/B Cell Receptor Signaling Pathway.BioMed research international · 2022Article
- Targeting AhR as a Novel Therapeutic Modality against Inflammatory Diseases.International journal of molecular sciences · 2021Review
- Cyproterone acetate acts as a disruptor of the aryl hydrocarbon receptor.Scientific reports · 2021Article
- AhR and Cancer: From Gene Profiling to Targeted Therapy.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor. Triple negative breast cancer (TNBC) is the most aggressive breast cancer subtype. TNBC expresses AHR and AHR ligands have anti-cancer activity in TNBC. The aggressiveness of TNBC is due in part to JAG1-NOTCH1 signaling. ITE is a putative endogenous AHR ligand. We show that ITE reduces the expression of JAG1 the amount of Notch 1 intracellular domain (NICD1) and the phosphorylation of STAT3 (at tyrosine 705) in TNBC MDA-MB-231 cells. The STAT3 inhibitor STATTIC also reduced JAG1. STAT3, thus, mediates regulation of JAG1 in MDA-MB-231 cells. Reducing the expression of JAG1 with short interfering RNA decreases the growth, migration and invasiveness of MDA-MB-231 cells. JAG1, therefore, has cellular effects in MDA-MB-231 cells under basal conditions. We consequently evaluated if exposing cells to greater amounts of JAG1 would counteract ITE cellular effects in MDA-MB-231 cells. The results show that JAG1 does not counteract the cellular effects of ITE. JAG1, thus, has no effect on growth or invasiveness in MDA-MB-231 cells treated with ITE. JAG1, therefore, has context dependent roles in MDA-MB-231 cells (basal versus ITE treatment). The results also show that other pathways, not inhibition of the JAG1-NOTCH1 pathway, are important for mediating the growth and invasive inhibitory effect of ITE on MDA-MB-231 cells.
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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.