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已发表论文
复方中药抗胃腺癌活性成分和分子靶点识别：网络药理学方法
Received 26 June 2025
Accepted for publication 21 January 2026
Published 29 January 2026 Volume 2026:19 549743
DOI https://doi.org/10.2147/IJGM.S549743
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Ching-Hsien Chen
Lei Liu,1 Yi Liu,2 Min Wu1
1Central Laboratory, Shaanxi Provincial People’s Hospital, Xi’an, Shaanxi, People’s Republic of China; 2Department of Oncology, Shaanxi Provincial People’s Hospital, Xi’an, Shaanxi, People’s Republic of China
Correspondence: Min Wu, Central Laboratory, Shaanxi Provincial People’s Hospital, 256 West Friendship Road, Xi’an, Shaanxi, 710068, People’s Republic of China, Tel +86029-85251331-2610, Email wumin175@spph-sx.ac.cn Yi Liu, Department of Oncology, Shaanxi Provincial People’s Hospital, 256 West Friendship Road, Xi’an, Shaanxi, 710068, People’s Republic of China, Tel +86029-85251331, Email liuyi@spph-sx.ac.cn
Background: The therapeutic effects of compound herbs (Radix Paeoniae Rubra, Radix Cirsii Japonici, Gentianae Radix Et Rhizoma, and Cardeniae Fructus) on stomach adenocarcinoma (STAD) remain unclear.
Methods: Active ingredients and their targets from the herbal combination were obtained using the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database. STAD-related targets were collected from the GeneCards database, and the TCGA-STAD dataset was downloaded from The Cancer Genome Atlas (TCGA) database. Differentially expressed genes (DEGs) between STAD and normal tissues were screened. The intersection of DEGs, drug targets, and STAD-related targets was taken to determine key targets. A protein–protein interaction (PPI) network was built and hub genes were identified. Functional enrichment analysis and molecular docking of the hub genes were performed. The Cell Counting Kit-8 (CCK8) assay was used to evaluate the effects of the active ingredients on the proliferation of Stomach Gastric Carcinoma cell line 7901 (SGC-7901) and MaKuNo cell line 45 (MKN-45) cells. The Transwell assay was used to evaluate the effect of quercetin on the migration ability of SGC-7901 and MKN-45 cells.
Results: A total of 67 key targets were obtained, among which five hub genes—ESR1 (Estrogen receptor 1), FOS (FBJ murine osteosarcoma viral oncogene homolog), HSP90AA199 (Heat shock protein 90 alpha family class A member 1), JUN (Avian sarcoma virus 17 oncogene homolog), and MMP9 (Matrix Metallopeptidase 9)—were identified. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated that these hub genes were significantly associated with the T Helper 17 (Th17) Cell differentiation pathway. Molecular docking predictions suggested that active ingredients such as quercetin could bind effectively to the hub genes, with quercetin showing the strongest binding affinity to FOS. Cell experiments further confirmed that quercetin exhibited the most potent inhibitory effect on the proliferation of STAD cells, with a half-maximal inhibitory concentration (IC50) value of 4 μM. Furthermore, quercetin can significantly inhibit the migration of SGC-7901 and MKN-45 cells.
Conclusion: This study identified five key targets and active compounds in herbal compounds for STAD treatment. These results suggest that quercetin may inhibit STAD progression by targeting FOS, and may have therapeutic potential.
Keywords: stomach adenocarcinoma, compound herbs, molecular docking, bioinformatics, quercetin
1Central Laboratory, Shaanxi Provincial People’s Hospital, Xi’an, Shaanxi, People’s Republic of China; 2Department of Oncology, Shaanxi Provincial People’s Hospital, Xi’an, Shaanxi, People’s Republic of China
Correspondence: Min Wu, Central Laboratory, Shaanxi Provincial People’s Hospital, 256 West Friendship Road, Xi’an, Shaanxi, 710068, People’s Republic of China, Tel +86029-85251331-2610, Email wumin175@spph-sx.ac.cn Yi Liu, Department of Oncology, Shaanxi Provincial People’s Hospital, 256 West Friendship Road, Xi’an, Shaanxi, 710068, People’s Republic of China, Tel +86029-85251331, Email liuyi@spph-sx.ac.cn
Background: The therapeutic effects of compound herbs (Radix Paeoniae Rubra, Radix Cirsii Japonici, Gentianae Radix Et Rhizoma, and Cardeniae Fructus) on stomach adenocarcinoma (STAD) remain unclear.
Methods: Active ingredients and their targets from the herbal combination were obtained using the Traditional Chinese Medicine Systems Pharmacology (TCMSP) database. STAD-related targets were collected from the GeneCards database, and the TCGA-STAD dataset was downloaded from The Cancer Genome Atlas (TCGA) database. Differentially expressed genes (DEGs) between STAD and normal tissues were screened. The intersection of DEGs, drug targets, and STAD-related targets was taken to determine key targets. A protein–protein interaction (PPI) network was built and hub genes were identified. Functional enrichment analysis and molecular docking of the hub genes were performed. The Cell Counting Kit-8 (CCK8) assay was used to evaluate the effects of the active ingredients on the proliferation of Stomach Gastric Carcinoma cell line 7901 (SGC-7901) and MaKuNo cell line 45 (MKN-45) cells. The Transwell assay was used to evaluate the effect of quercetin on the migration ability of SGC-7901 and MKN-45 cells.
Results: A total of 67 key targets were obtained, among which five hub genes—ESR1 (Estrogen receptor 1), FOS (FBJ murine osteosarcoma viral oncogene homolog), HSP90AA199 (Heat shock protein 90 alpha family class A member 1), JUN (Avian sarcoma virus 17 oncogene homolog), and MMP9 (Matrix Metallopeptidase 9)—were identified. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated that these hub genes were significantly associated with the T Helper 17 (Th17) Cell differentiation pathway. Molecular docking predictions suggested that active ingredients such as quercetin could bind effectively to the hub genes, with quercetin showing the strongest binding affinity to FOS. Cell experiments further confirmed that quercetin exhibited the most potent inhibitory effect on the proliferation of STAD cells, with a half-maximal inhibitory concentration (IC50) value of 4 μM. Furthermore, quercetin can significantly inhibit the migration of SGC-7901 and MKN-45 cells.
Conclusion: This study identified five key targets and active compounds in herbal compounds for STAD treatment. These results suggest that quercetin may inhibit STAD progression by targeting FOS, and may have therapeutic potential.
Keywords: stomach adenocarcinoma, compound herbs, molecular docking, bioinformatics, quercetin