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Article | Open Access

Gallic acid suppresses esophageal squamous cell carcinoma progression and enhances cisplatin chemosensitivity through IL-6/STAT3/Notch pathway

NURAN BEDOLLA#, HAO WU#, LINYU LIU, XUETING LIU, YANLI REN( )
College of Biological Sciences and Technology, YiLi Normal University, Yining, 835000, China

#These two authors contributed equally to this work

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Highlights:

1. Gallic acid (GA) inhibits proliferation and induces apoptosis of ESCC cells.

2. Interleukin-6 (IL-6) intervention activates the Signal transducer and activator of transcription 3 (STAT3)/Notch pathway and it promotes ESCC malignant progression and increases cell resistance to cisplatin (DDP).

3. GA modulates the IL-6/STAT3/Notch pathway, inhibits ESCC malignant progression, and promotes oxidative stress.

4. The combination of GA and DDP shows increased sensitivity of ESCC cells to DDP.

5. The IL-6/STAT3/Notch pathway is suppressed by GA, leading to increased sensitivity of ESCC cells to DDP.

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 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.

Keywords

Gallic acid (GA)CisplatinEsophageal cancerInterleukin-6 (IL-6)Chemotherapy sensitivitySignal transducer and activator of transcription 3 (STAT3)/Notch pathway

References

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Oncology Research
Volume 33 Issue 6,
May 2025
Pages 1473-1484
DOI: 10.32604/or.2025.060151

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Cite this article:
BEDOLLA N, WU H, LIU L, et al. Gallic acid suppresses esophageal squamous cell carcinoma progression and enhances cisplatin chemosensitivity through IL-6/STAT3/Notch pathway. Oncology Research, 2025, 33(6): 1473-1484. https://doi.org/10.32604/or.2025.060151

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Received: 25 October 2024
Accepted: 16 January 2025
Published: 29 May 2025
© The Author 2024.

This work is licensed under a Creative Commons Attribution 4.0 International License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.