Evidence map›Paper›PMID 40837755›Full record

ArticleWorld journal of gastrointestinal oncology2025

Qige San regulates paclitaxel resistance in esophageal cancer by targeting ferroptosis.

Jie Song, Wen-Ying Guo, Le-Bo Sun

Abstract read
In one paragraph

Article in World journal of gastrointestinal oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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.

2 · The registry

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3 · Its place in the literature

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Jie SongDepartment of Cardiothoracic Surgery, Ningbo Medical Center Lihuili Hospital of Ningbo University, Ningbo 315041, Zhejiang Province, China.
Wen-Ying GuoDepartment of Gastroenterology, Ningbo Medical Center Lihuili Hospital, Ningbo 315000, Zhejiang Province, China.
Le-Bo SunDepartment of Cardiothoracic Surgery, Ningbo Medical Center Lihuili Hospital of Ningbo University, Ningbo 315041, Zhejiang Province, China. sunlebo0910@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAbnormal 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.

aimTo investigate the effects and regulatory mechanisms involved in QG-targeted PTX-resistant esophageal cancer cells.

methodsCell viability was assessed using the Cell Counting Kit-8 assay. Ferroptosis was evaluated by analyzing lipid reactive oxygen species accumulation and the Fe

resultsTreatment 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.

conclusionQG could repress the resistance of esophageal cancer cells to PTX

Indexed as

Esophageal cancerFerroptosisNetwork pharmacologyPaclitaxel resistanceQige San

Identifiers

PMID40837755
PMCPMC12362534

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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 OpenQuestion graph.