Open Access

ARTICLE

Network pharmacology and molecular docking identify mechanisms of medicinal plant-derived 1,2,3,4,6-penta-O-galloyl-beta-D-glucose treating gastric cancer

MAN REN^1,2,3,#, YUAN YANG^1,2,#, DAN LI⁴, NANNAN ZHAO⁵, YUPING WANG^2,6,*, YONGNING ZHOU^2,6,*

1 The First Clinical Medical College, Lanzhou University, Lanzhou, 730000, China
2 Gansu Key Laboratory of Gastroenterology, Lanzhou University, Lanzhou, 730000, China
3 Department of Geriatrics Gerontology, The First Hospital of Lanzhou University, Lanzhou, 730000, China
4 Office of National Drug Clinical Trial Institutions, The First Hospital of Lanzhou University, Lanzhou, 730000, China
5 School of Pharmacy, Lanzhou University, Lanzhou, 730000, China
6 Department of Gastroenterology, The First Hospital of Lanzhou University, Lanzhou, 730000, China

* Corresponding Authors: YUPING WANG. Email: ; YONGNING ZHOU. Email:

BIOCELL 2023, 47(5), 977-989. https://doi.org/10.32604/biocell.2023.028402

Received 16 December 2022; Accepted 17 January 2023; Issue published 10 April 2023

Abstract

Background: 1,2,3,4,6-penta-O-galloyl-beta-D-glucose (PGG) is a natural polyphenolic compound derived from multiple medicinal plants with favorable anticancer activity. Methods: In this study, the mechanisms of PGG against gastric cancer were explored through network pharmacology and molecular docking. First, the targets of PGG were searched in the Herbal Ingredients’ Targets (HIT), Similarity Ensemble Approach (SEA), and Super-PRED databases. The potential targets related to gastric cancer were predicted from the Human Gene Database (GeneCards) and DisGeNET databases. The intersecting targets of PGG and gastric cancer were obtained by Venn diagram and then subjected to protein-protein interaction analysis to screen hub targets. Functional and pathway enrichment of hub targets were analyzed through Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway databases. The differential expression and survival analysis of hub targets in gastric cancer were performed based on The Cancer Genome Atlas database. Finally, the affinity of PGG with hub targets was visualized by molecular docking. Results: Three hub targets were screened, including mitogen-activated protein kinase 14 (MAPK14), BCL2 like 1 (BCL2L1), and vascular endothelial growth factor A (VEGFA). MAPK14 had a higher expression, while BCL2L1 and VEGFA had lower expression in gastric cancer than in normal conditions. Enrichment analysis indicated enrichment of these hub targets in MAPK, neurotrophin, programmed death-ligand 1 (PD-L1) checkpoint, phosphatidylinositol 3-kinases/protein kinase B (PI3K-Akt), Ras, and hypoxia-inducible factor-1 (HIF-1) signaling pathways. Conclusion: Therefore, network pharmacology and molecular docking analyses revealed that PGG exerts a therapeutic efficacy on gastric cancer by multiple targets (MAPK14, BCL2L1, and VEGFA) and pathways (MAPK, PD-L1 checkpoint, PI3K-Akt, Ras, and HIF-1 pathways).

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Supplementary Material

Supplementary Material File

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