ArticleWorld journal of gastrointestinal oncology2025
Molecular mechanism of modified Yigong San formula against colorectal cancer
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. Cited by 1 paper.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Combinational Inhibition of the eIF4F Complex, AKT1, and EZH2 Enhances Anticancer Effects in BRAFOncology research · 2026Article
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Authors and funding
5 authors.
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Abstract
backgroundColorectal cancer (CRC) is a malignant tumor characterized by high global incidence and mortality rates. Contemporary therapeutic modalities remain limited by suboptimal efficacy and adverse effects, thereby necessitating the pursuit of more efficacious treatment strategies. Within traditional Chinese medicine, spleen deficiency is regarded as a central pathogenic mechanism in CRC, persisting throughout the entire disease course.
aimTo elucidate the mechanism by which modified Yigong San confers therapeutic efficacy against CRC, potentially exerting its effects through apoptosis regulation mediated by the enhancer of zeste homolog 2 (EZH2)/methyltransferase-like 3 (METTL3)/SRY-box transcription factor 4 (SOX4) axis.
methodsIn the clinical study, CRC tissues and corresponding adjacent normal samples that fulfilled inclusion criteria were procured. Quantitative reverse transcription polymerase chain reaction was employed to determine the transcriptional expression of
resultsThe clinical findings demonstrated significantly elevated transcriptional levels of
conclusionModified Yigong San exhibits both preventive and therapeutic potential against CRC, likely mediated through the regulation of apoptosis
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