ArticleScientific reports2025
Investigating the PI3K/AKT/mTOR axis in Buzhong Yiqi Decoction's anti-colorectal cancer activity.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Macrophage-associated kinase signaling in atherosclerosis - a systematic review.Cell communication and signaling : CCS · 2026Pooled it
- Astragaloside II suppresses colorectal cancer progression by upregulating LGALS4 expression.Journal of molecular histology · 2026Article
- Poricoic Acid A Attenuates Osteoarthritis Progression by Stabilizing PTEN and Suppressing PI3K/AKT Signaling.International journal of molecular sciences · 2026Article
- Metabolites of Astragalus membranaceus and their pro-apoptotic and cytotoxic activities: insights into targeted metabolic pathways.Frontiers in pharmacology · 2025Review
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6 authors.
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Abstract
Buzhong Yiqi Decoction (BZYQD) is a traditional Chinese medicine renowned for its anti-colorectal cancer (CRC) properties. However, the bioactive components and mechanisms of BZYQD against CRC remain unknown. In this study, LC-MS was used to analyze the chemical composition of BZYQD. Next, the network pharmacology and molecular docking was used to investigate the core components and targets of BZYQD against CRC. Finally, we experimentally validated the potential mechanism of BZYQD against CRC through in vitro studies. Our results identified 26 chemical components in the BZYQD; 75 "hithubs" targets were screened by network pharmacology, and mainly involving pathways such as including pathways in cancer, P13K-Akt signaling pathway, proteoglycans in cancer, kaposi sarcoma-associated herpesvirus, and lipid and atherosclerosis signaling pathways. Based on the number of "hithubs" targets in the key pathways, the two most critical targets including AKT1 and PIK3CA were selected. The component-target network results indicated that astragaloside IV, gancaonin A, quercetin, poricoic acid A, and licoisoflavanone are key anti-CRC components in BZYQD. Molecular docking showed a strong binding affinity between these components and targets. The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway emerged as the primary target of BZYQD. Further in vitro studies confirmed that BZYQD's anti-CRC activity is mediated through the PI3K/AKT/mTOR axis and influences macrophage polarization. BZYQD exerts its therapeutic effects on CRC through multiple components, targets, and pathways. Our study elucidates the effective components and molecular mechanisms of BZYQD in CRC treatment and provides preliminary validation through molecular docking and experimental studies.
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