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没食子酸通过IL-6/STAT3/Notch信号通路抑制食管鳞状细胞癌进展并增强顺铂化疗敏感性。

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

作者信息

Bedolla Nuran, Wu Hao, Liu Linyu, Liu Xueting, Ren Yanli

机构信息

College of Biological Sciences and Technology, YiLi Normal University, Yining, 835000, China.

出版信息

Oncol Res. 2025 May 29;33(6):1473-1484. doi: 10.32604/or.2025.060151. eCollection 2025.

DOI:10.32604/or.2025.060151
PMID:40486873
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12144628/
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 and .

CONCLUSION

GA suppresses the malignant progression of ESCC and enhances cell sensitivity to DDP by hindering the IL-6/STAT3/Notch pathway.

摘要

背景

没食子酸（GA）是一种植物来源的多酚，具有多种生物学功能，如减轻炎症和抗肿瘤。目前，GA对食管鳞状细胞癌（ESCC）细胞顺铂（DDP）耐药性的影响尚不清楚。

方法

细胞计数试剂盒-8法检测GA对KYSE30和TE-1细胞活力的影响。5-乙炔基-2'-脱氧尿苷和末端脱氧核苷酸转移酶介导的缺口末端标记染色检测细胞增殖和凋亡。克隆形成试验、流式细胞术、羧基荧光素二乙酸琥珀酰亚胺酯荧光探针和Transwell试验测定细胞生物学特性，2',7'-二氯荧光素二乙酸酯（DCFH-DA）荧光探针检测氧化应激水平。通过蛋白质免疫印迹法检测GA和/或白细胞介素-6（IL-6）干预后信号转导和转录激活因子3（STAT3）/Notch通路蛋白水平。此外，在裸鼠中建立皮下移植瘤模型。

结果

GA对细胞增殖有抑制作用，并导致KYSE30和TE-1细胞凋亡。IL-6干预激活STAT3/Notch通路，促进ESCC细胞的恶性生物学特性。相反，GA减弱了IL-6的作用，而STAT3或Notch抑制剂进一步增强了GA的作用，表明GA抑制了IL-6/STAT3/Notch通路。不仅如此，GA还促进氧化应激并增强细胞对DDP的敏感性。

结论

GA通过阻碍IL-6/STAT3/Notch通路抑制ESCC的恶性进展并增强细胞对DDP的敏感性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1854/12144628/a31396aa3914/OncolRes-33-60151-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1854/12144628/c02bbe6066ec/OncolRes-33-60151-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1854/12144628/c1a667d6071a/OncolRes-33-60151-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1854/12144628/3d8c7ec1e9c3/OncolRes-33-60151-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1854/12144628/438d0dda01c5/OncolRes-33-60151-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1854/12144628/8bc0fe104061/OncolRes-33-60151-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1854/12144628/a31396aa3914/OncolRes-33-60151-f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1854/12144628/c02bbe6066ec/OncolRes-33-60151-f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1854/12144628/c1a667d6071a/OncolRes-33-60151-f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1854/12144628/3d8c7ec1e9c3/OncolRes-33-60151-f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1854/12144628/438d0dda01c5/OncolRes-33-60151-f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1854/12144628/8bc0fe104061/OncolRes-33-60151-f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1854/12144628/a31396aa3914/OncolRes-33-60151-f006.jpg

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