ArticleChinese medicine2025
Huqi formula suppresses hepatocellular carcinoma growth by modulating the PI3K/AKT/mTOR pathway and promoting T cell infiltration.
Article in Chinese medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Knowledge Mapping and Frontier Evolution of Traditional Medicine in Hepatocellular Carcinoma Research: A Bibliometric Analysis.Journal of hepatocellular carcinoma · 2026Review
- Oridonin attenuates TLR4-driven inflammation and autophagy in LPS-stimulated enteric glial cells: anFrontiers in cellular neuroscience · 2026Article
- How Traditional Chinese Medicine Works: Biological Mechanisms and Clinical Evidence for Hepatocellular Carcinoma Treatment.Drug design, development and therapy · 2026Review
- Decoding the Mechanisms of Hepatocellular Carcinoma Cancer Stem Cells and Identifying Potential Therapeutic Strategies Based on Single-cell Omics.Cancer genomics & proteomicsArticle
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Authors and funding
17 authors.
Funding
Abstract
backgroundHepatocellular carcinoma (HCC) poses ongoing difficulties for public health systems due to its high incidence and poor prognosis. Huqi formula (HQF), a well-known prescription in traditional Chinese medicine, has demonstrated notable clinical effectiveness in the treatment of HCC. However, the mechanisms underlying its therapeutic effects have yet to be completely elucidated. PURPOSE: This study aimed to investigate the anti-HCC effects of HQF and its underlying mechanisms.
methodsChemical profiling and quantification of HQF were conducted by LC-MS and HPLC. Orthotopic and subcutaneous tumor models were established through hydrodynamic injection of Akt/Nras plasmids and subcutaneous injection of c-Met/sgPten cells, respectively, to evaluate the therapeutic effects of HQF on HCC. Network pharmacology, RNA-Seq, molecular docking, Western blot, and flow cytometry were employed to assess the anti-HCC mechanisms.
resultsLC-MS analysis identified 41 components, with HPLC quantification showing salvianolic acid B as the most abundant compound (0.303%). In Akt/Nras and c-Met/sgPten-induced HCC models, HQF significantly reduced tissue damage, improved liver function, and inhibited HCC progression. Mechanistic studies revealed that HQF induced apoptosis in HCC cells by downregulating p-PI3K, p-AKT, and p-mTOR expression, with molecular docking indicating the strongest binding affinity between salvianolic acid B and PI3K. HQF further enhanced CD4
conclusionHQF demonstrated significant anti-HCC effects and a synergistic effect with PD-1, could be used as an alternative therapeutic agent for HCC.
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