Open Access
ARTICLE
Ampelopsin Inhibits Breast Cancer Glucose Metabolism Reprogramming Based on Network Pharmacology and Molecular Docking
Rong Zeng1,#, Lin Liu1,2,#, Jingshan Zhao1,2,3,#, Wenmei Zhang3, Guohong Zhang1, Yunfeng Li1,2,*
1
Hebei Key Laboratory of Chinese Medicine Research on Cardiocerebrovascular Disease, Hebei University of Chinese Medicine,
Shijiazhuang, 050200, China
2
Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei University of Chinese Medicine,
Shijiazhuang, 050200, China
3
College of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang, 050200, China
* Corresponding Author: Yunfeng Li. Email:
# These authors contributed equally to this work
Oncologie 2022, 24(3), 483-498. https://doi.org/10.32604/oncologie.2022.025148
Received 24 June 2022; Accepted 02 August 2022; Issue published 19 September 2022
Abstract
Background: Breast cancer (BC) is the most frequent type of gynecology tumors with high morbidity and mortality. Ampelopsin, the main active compound of
Ampelopsis grossedentata, exerts an anti-tumor effect on a variety of cancers. However, the anti-cancer role of ampelopsin in BC remains unclear. The aim of this study is to
explore the mechanism of ampelopsin against breast cancer.
Materials and Methods: The target genes of ampelopsin in the treatment of breast cancer were determined and analyzed by network pharmacology and molecular
docking. Cytoscape software was used to identify the core target genes and construct a protein–protein interaction
(PPI) network. Discovery Studio software was used to perform the molecular docking of ampelopsin and core
genes and glycolytic metabolic enzymes.
Results: In total, 25 potential target genes of ampelopsin were screened
out. The core target genes of ampelopsin against breast cancer were
AKT1,
ESR1,
ESR2,
NCOA1,
HSP90AA1,
NCOA2,
BECN1,
COMT,
HMOX1, and
CDK6, with AKT1, ESR1 and ESR2 considered as the key target proteins.
Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that ampelopsin inhibited breast cancer via
modulating the estrogen signaling pathway, apoptosis regulation, carbohydrate metabolism, and inflammation.
Molecular docking analysis showed that ampelopsin possessed a stable binding ability to regulate the three target
proteins and glycolytic metabolic enzymes such as ALDOA and LDHA.
Conclusions: Ampelopsin may inhibit
the proliferation of breast cancer cells by acting on AKT and estrogen-related glucose metabolic pathways and
inhibiting the enzymes involved in glycolysis and oxidative phosphorylation.
Keywords
Cite This Article
Zeng, R., Liu, L., Zhao, J., Zhang, W., Zhang, G. et al. (2022). Ampelopsin Inhibits Breast Cancer Glucose Metabolism Reprogramming Based on Network Pharmacology and Molecular Docking.
Oncologie, 24(3), 483–498.