Network Pharmacology, Molecular Docking and Experimental Verification to Explore the Mechanism of Chicoric Acid against Hepatocellular Carcinoma

To investigate the inhibitory effects and mechanisms of chicoric acid (CA) on hepatocellular carcinoma (HCC), this study employed an integrated approach combining network pharmacology, molecular docking, and experimental validation to analyze its multi-target mechanism systematically. Swiss Target P...

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Main Authors: Wenqian XU, Liangliang ZHANG, Yiping ZHAO, He QIAN, Jianguo XU
Format: Article
Language:zho
Published: The editorial department of Science and Technology of Food Industry 2025-09-01
Series:Shipin gongye ke-ji
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Online Access:http://www.spgykj.com/cn/article/doi/10.13386/j.issn1002-0306.2025020219
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author Wenqian XU
Liangliang ZHANG
Yiping ZHAO
He QIAN
Jianguo XU
author_facet Wenqian XU
Liangliang ZHANG
Yiping ZHAO
He QIAN
Jianguo XU
author_sort Wenqian XU
collection DOAJ
description To investigate the inhibitory effects and mechanisms of chicoric acid (CA) on hepatocellular carcinoma (HCC), this study employed an integrated approach combining network pharmacology, molecular docking, and experimental validation to analyze its multi-target mechanism systematically. Swiss Target Prediction database was used to predict the potential target of CA, while Liverome and Onco DB.HCC databases were integrated to screen HCC-related targets. The protein interaction network was constructed using Cytoscape, followed by GO (Gene Ontology) biological function and KEGG (Kyoto Encyclopedia of Genes and Genes) pathway analyses via the DAVID database. Molecular docking between CA and core targets was performed using AutoDock. Finally, in vitro Hepa1-6 cell experiments were conducted to evaluate the inhibitory effect of CA on HCC cell viability and migration by CCK8 assay, cell scratch test, and mRNA analysis of key genes. The key pathways predicted by network pharmacology were verified by western blotting. In this study, 103 potential targets of CA, 1007 targets of HCC, and 31 intersection targets were screened. The core targets involved serine/threonine kinase 1 (AKT1) and phosphatidylinositol 4, 5-diphosphate 3-kinase catalytic subunit α (PIK3CA). GO enrichment analysis highlighted processes such as cytoplasm, protein binding, and protein hydrolysis, while KEGG analysis revealed enrichment in the PI3K-Akt signaling pathway and cancer pathway. Molecular docking results showed that CA had good binding activity with the key targets PI3K and AKT. In vitro cell experiments demonstrated that CA significantly inhibited the proliferation and migration capabilities of HCC cells, downregulated the mRNA expression of tumor growth-related genes Egfr and Mmp2, and reduced the phosphorylation levels of PI3K and AKT protein. While PI3K-Akt pathway agonists induced the proliferation and migration of Hepa1-6 cells, CA effectively suppressed the progression of HCC cells and downregulated the expression of p-PI3K and p-AKT. This study preliminarily revealed that CA inhibited the proliferation and migration of HCC cells by regulating the PI3K-Akt signaling pathway. The integration of network pharmacology, molecular docking, and in vitro experimental validation provides a scientific basis for an in-depth study of the mechanism of action of CA against HCC.
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spelling doaj-art-e35509afc0654a608f2575d5d5b934b92025-08-26T01:30:45ZzhoThe editorial department of Science and Technology of Food IndustryShipin gongye ke-ji1002-03062025-09-01461743644610.13386/j.issn1002-0306.20250202192025020219-17Network Pharmacology, Molecular Docking and Experimental Verification to Explore the Mechanism of Chicoric Acid against Hepatocellular CarcinomaWenqian XU0Liangliang ZHANG1Yiping ZHAO2He QIAN3Jianguo XU4College of Food Science, Shanxi Normal University, Taiyuan 030006, ChinaCollege of Food Science, Shanxi Normal University, Taiyuan 030006, ChinaCollege of Food Science, Shanxi Normal University, Taiyuan 030006, ChinaSchool of Food Science, Jiangnan University, Wuxi 214122, ChinaCollege of Food Science, Shanxi Normal University, Taiyuan 030006, ChinaTo investigate the inhibitory effects and mechanisms of chicoric acid (CA) on hepatocellular carcinoma (HCC), this study employed an integrated approach combining network pharmacology, molecular docking, and experimental validation to analyze its multi-target mechanism systematically. Swiss Target Prediction database was used to predict the potential target of CA, while Liverome and Onco DB.HCC databases were integrated to screen HCC-related targets. The protein interaction network was constructed using Cytoscape, followed by GO (Gene Ontology) biological function and KEGG (Kyoto Encyclopedia of Genes and Genes) pathway analyses via the DAVID database. Molecular docking between CA and core targets was performed using AutoDock. Finally, in vitro Hepa1-6 cell experiments were conducted to evaluate the inhibitory effect of CA on HCC cell viability and migration by CCK8 assay, cell scratch test, and mRNA analysis of key genes. The key pathways predicted by network pharmacology were verified by western blotting. In this study, 103 potential targets of CA, 1007 targets of HCC, and 31 intersection targets were screened. The core targets involved serine/threonine kinase 1 (AKT1) and phosphatidylinositol 4, 5-diphosphate 3-kinase catalytic subunit α (PIK3CA). GO enrichment analysis highlighted processes such as cytoplasm, protein binding, and protein hydrolysis, while KEGG analysis revealed enrichment in the PI3K-Akt signaling pathway and cancer pathway. Molecular docking results showed that CA had good binding activity with the key targets PI3K and AKT. In vitro cell experiments demonstrated that CA significantly inhibited the proliferation and migration capabilities of HCC cells, downregulated the mRNA expression of tumor growth-related genes Egfr and Mmp2, and reduced the phosphorylation levels of PI3K and AKT protein. While PI3K-Akt pathway agonists induced the proliferation and migration of Hepa1-6 cells, CA effectively suppressed the progression of HCC cells and downregulated the expression of p-PI3K and p-AKT. This study preliminarily revealed that CA inhibited the proliferation and migration of HCC cells by regulating the PI3K-Akt signaling pathway. The integration of network pharmacology, molecular docking, and in vitro experimental validation provides a scientific basis for an in-depth study of the mechanism of action of CA against HCC.http://www.spgykj.com/cn/article/doi/10.13386/j.issn1002-0306.2025020219chicoric acidhepatocellular carcinomanetwork pharmacologyexperimental verificationpi3k-akt signaling pathway
spellingShingle Wenqian XU
Liangliang ZHANG
Yiping ZHAO
He QIAN
Jianguo XU
Network Pharmacology, Molecular Docking and Experimental Verification to Explore the Mechanism of Chicoric Acid against Hepatocellular Carcinoma
Shipin gongye ke-ji
chicoric acid
hepatocellular carcinoma
network pharmacology
experimental verification
pi3k-akt signaling pathway
title Network Pharmacology, Molecular Docking and Experimental Verification to Explore the Mechanism of Chicoric Acid against Hepatocellular Carcinoma
title_full Network Pharmacology, Molecular Docking and Experimental Verification to Explore the Mechanism of Chicoric Acid against Hepatocellular Carcinoma
title_fullStr Network Pharmacology, Molecular Docking and Experimental Verification to Explore the Mechanism of Chicoric Acid against Hepatocellular Carcinoma
title_full_unstemmed Network Pharmacology, Molecular Docking and Experimental Verification to Explore the Mechanism of Chicoric Acid against Hepatocellular Carcinoma
title_short Network Pharmacology, Molecular Docking and Experimental Verification to Explore the Mechanism of Chicoric Acid against Hepatocellular Carcinoma
title_sort network pharmacology molecular docking and experimental verification to explore the mechanism of chicoric acid against hepatocellular carcinoma
topic chicoric acid
hepatocellular carcinoma
network pharmacology
experimental verification
pi3k-akt signaling pathway
url http://www.spgykj.com/cn/article/doi/10.13386/j.issn1002-0306.2025020219
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