ArticleDiscover oncology2026
Zerumbone mediated CD1d inhibition suppresses epithelial to mesenchymal transition in triple negative breast cancer.
Article in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Thymoquinone Enhances Tamoxifen Efficacy Against Triple-Negative Breast Cancer by Targeting EMT Signaling.International journal of breast cancer · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Triple-negative breast cancer (TNBC) is characterized by aggressive metastatic behavior driven through epithelial-to-mesenchymal transition (EMT). CD1d, a non-classical MHC molecule, modulates immune responses via Natural Killer T (NKT) cells and is implicated in tumor progression. This study examines the effect of CD1d inhibition on EMT in TNBC. We demonstrate that Zerumbone (ZER, 20 µM), a phytochemical, downregulates CD1d, reducing EMT markers, cell migration, and adhesion in MDA-MB-468 and MDA-MB-231 TNBC cell lines. Conversely, CD1d upregulation by α-galactosylceramide (AGC, 2 µM) and thymosin α-1 (TA, 2 µM) promotes EMT, enhances migration and adhesion. Immunofluorescence and Western blot analyses confirmed ZER suppresses CD1d, vimentin, N-cadherin, and FASN, while increasing E-cadherin, indicating mesenchymal-to-epithelial transition (MET). AGC and TA elevate CD1d and EMT markers. Molecular docking and dynamics simulations show ZER’s stable binding to CD1d (-8.13 kcal/mol), supporting the in vitro data and it is predicted to act as a potential CD1d antagonist. These findings suggest that CD1d inhibition may represent a potential strategy to attenuate EMT associated phenotypes in TNBC.
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What Socratic holds
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 Socratic graph.