Song J, Guo WY, Sun LB. Qige San regulates paclitaxel resistance in esophageal cancer by targeting ferroptosis. World J Gastrointest Oncol 2025; 17(8): 106783 [DOI: 10.4251/wjgo.v17.i8.106783]
Corresponding Author of This Article
Le-Bo Sun, Department of Cardiothoracic Surgery, Ningbo Medical Center Lihuili Hospital of Ningbo University, No. 57 Xingning Road, Ningbo 315041, Zhejiang Province, China. sunlebo0910@163.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastrointest Oncol. Aug 15, 2025; 17(8): 106783 Published online Aug 15, 2025. doi: 10.4251/wjgo.v17.i8.106783
Qige San regulates paclitaxel resistance in esophageal cancer by targeting ferroptosis
Jie Song, Wen-Ying Guo, Le-Bo Sun
Jie Song, Le-Bo Sun, Department of Cardiothoracic Surgery, Ningbo Medical Center Lihuili Hospital of Ningbo University, Ningbo 315041, Zhejiang Province, China
Wen-Ying Guo, Department of Gastroenterology, Ningbo Medical Center Lihuili Hospital, Ningbo 315000, Zhejiang Province, China
Author contributions: Song J designed the research study; Guo WY performed the research; Sun LB conducted experiments and analyzed the data; All authors contributed to editorial changes in the manuscript and read and approved the final manuscript.
Supported by Zhejiang Traditional Chinese Medicine Administration, No. 2024ZL944.
Institutional review board statement: This study was approved by the Ethics Committee of Ningbo Medical Center Lihuili Hospital of Ningbo University, No. LHL159329.
Conflict-of-interest statement: All authors report no relevant conflicts of interest for this article.
Data sharing statement: No additional data are available.
Open Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Le-Bo Sun, Department of Cardiothoracic Surgery, Ningbo Medical Center Lihuili Hospital of Ningbo University, No. 57 Xingning Road, Ningbo 315041, Zhejiang Province, China. sunlebo0910@163.com
Received: April 18, 2025 Revised: May 14, 2025 Accepted: July 7, 2025 Published online: August 15, 2025 Processing time: 117 Days and 15.7 Hours
Abstract
BACKGROUND
Abnormal iron metabolism plays a critical role in paclitaxel (PTX) resistance in esophageal cancer cells. Qige San (QG) is a traditional Chinese herbal formula that is reported to improve short-term therapeutic effects of esophageal cancer.
AIM
To investigate the effects and regulatory mechanisms involved in QG-targeted PTX-resistant esophageal cancer cells.
METHODS
Cell viability was assessed using the Cell Counting Kit-8 assay. Ferroptosis was evaluated by analyzing lipid reactive oxygen species accumulation and the Fe2+ concentration in PTX-resistant esophageal cancer cells. Expression of ferroptosis regulators was measured by western blot. Network pharmacology analysis was employed to identify potential targets of QG in PTX-resistant esophageal cancer cells.
RESULTS
Treatment with QG significantly suppressed the viability, proliferation, and migration of PTX-resistant esophageal cancer cells and simultaneously induced ferroptosis. The network pharmacology analysis identified the phosphoinositide 3-kinase (PI3K)/protein kinase B signaling pathway as the potential target of QG in PTX-resistant esophageal cancer cells. Activation of the PI3K pathway notably reversed the ferroptosis of PTX-resistant esophageal cancer cells that was induced by QG.
CONCLUSION
QG could repress the resistance of esophageal cancer cells to PTX via targeting the PI3K signaling pathway.
Core Tip: Abnormal iron metabolism plays a critical role in paclitaxel-resistance of esophageal cancer cells. Qige San (QG) is a traditional Chinese herbal formula that is reported to improve short-term therapeutic effects of esophageal cancer. We observed that QG could repress the resistance of esophageal cancer cells to paclitaxel via targeting the phosphoinositide 3-kinase/protein kinase B signaling pathway.
