Gallic acid suppresses esophageal squamous cell carcinoma progression and enhances cisplatin chemosensitivity through IL-6/STAT3/Notch pathway
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Updated: Jun 12, 2025
Evaluating the Effectiveness of Cancer Drug Sensitization In Vitro and In Vivo
Published on: February 6, 2015
Nuran Bedolla1, Hao Wu1, Linyu Liu1
1College of Biological Sciences and Technology, YiLi Normal University, Yining, 835000, China.
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 in vitro and in vivo.
Conclusion:
GA suppresses the malignant progression of ESCC and enhances cell sensitivity to DDP by hindering the IL-6/STAT3/Notch pathway.
Insights
Gallic acid (GA) combats esophageal squamous cell carcinoma (ESCC) progression and cisplatin (DDP) resistance by inhibiting the IL-6/STAT3/Notch pathway and increasing oxidative stress.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Gallic acid (GA), a polyphenol from plants, has anti-inflammatory and anti-tumor properties.
- The effect of GA on cisplatin (DDP) resistance in esophageal squamous cell carcinoma (ESCC) is not well understood.
Purpose of the Study:
- To investigate the impact of Gallic acid (GA) on the biological behavior of esophageal squamous cell carcinoma (ESCC) cells.
- To explore the underlying molecular mechanisms of GA's action, particularly its influence on the IL-6/STAT3/Notch pathway and DDP resistance.
Main Methods:
- Cell viability, proliferation, apoptosis, and migration assays were performed using KYSE30 and TE-1 ESCC cell lines.
- Oxidative stress levels were measured using DCFH-DA probes.
- Protein expression of the STAT3/Notch pathway was analyzed via Western blot.
- Tumorigenicity was assessed in a mouse xenograft model.
Main Results:
- Gallic acid (GA) suppressed ESCC cell proliferation and induced apoptosis.
- GA attenuated IL-6-induced activation of the STAT3/Notch pathway.
- GA treatment enhanced ESCC cell sensitivity to cisplatin (DDP) both in vitro and in vivo.
- GA promoted oxidative stress in ESCC cells.
Conclusions:
- Gallic acid (GA) inhibits the malignant progression of ESCC.
- GA enhances DDP sensitivity in ESCC by suppressing the IL-6/STAT3/Notch pathway.
- GA's ability to promote oxidative stress contributes to its therapeutic effects in ESCC.
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