ArticleOncology research2025
Gallic acid suppresses esophageal squamous cell carcinoma progression and enhances cisplatin chemosensitivity through IL-6/STAT3/Notch pathway.
Article in Oncology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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Who cites it
3 citing papers in PubMed.
- Gallic acid-driven core-shell nanovehicles enable intestinal adhesion and adipose retention for enhanced oral bioavailability of cholecalciferol.Drug delivery · 2026Article
- miR-335-3p acts as a tumor suppressor in esophageal squamous cell carcinoma and predicts favorable prognosis.Hereditas · 2026Article
- Targeting notch signaling pathway in esophageal cancer: from molecular insights to therapies.Oncology reviews · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Gallic acid (GA), a plant-derived polyphenol, possesses diverse biological functions such as reducing inflammation and against tumors. Currently, the influence of GA on the resistance of esophageal squamous cell carcinoma (ESCC) cells to cisplatin (DDP) is not well understood. Methods: Cell counting kit-8 assay examined how GA affected KYSE30 and TE-1 cell viability. 5-Ethynyl-2'-deoxyuridine and TdT-mediated dUTP Nick-End labeling staining detected cell proliferation and apoptosis. Clone formation assay, flow cytometry, Carboxyfluorescein diacetate succinimidyl ester fluorescent probes, and Transwell assay determined cell biological properties, and 2',7'-Dichlorofluorescin diacetate (DCFH-DA) fluorescent probes detected oxidative stress levels. Signal transducer and activator of transcription 3 (STAT3)/Notch pathway protein levels after GA and/or Interleukin-6 (IL-6) intervention were examined through Western blot. Furthermore, a model for subcutaneous graft tumors was established in nude mice. Results: GA exerted suppressive effects on cell proliferation, and caused apoptosis of KYSE30 and TE-1 cells. IL-6 intervention activated the STAT3/Notch pathway and promoted the malignant biological properties of ESCC cells. In contrast, GA attenuated the effects of IL-6, while STAT3 or Notch inhibitor further enhanced the effects of GA, suggesting that GA inhibited the IL-6/STAT3/Notch pathway. Not only that, GA promoted oxidative stress and enhanced cell sensitivity to DDP both Conclusion: GA suppresses the malignant progression of ESCC and enhances cell sensitivity to DDP by hindering the IL-6/STAT3/Notch pathway.
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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 Socratic graph.