@Article{oncologie.2022.025148,
AUTHOR = {Rong Zeng, Lin Liu, Jingshan Zhao, Wenmei Zhang, Guohong Zhang, Yunfeng Li},
TITLE = {Ampelopsin Inhibits Breast Cancer Glucose Metabolism Reprogramming Based on Network Pharmacology and Molecular Docking},
JOURNAL = {Oncologie},
VOLUME = {24},
YEAR = {2022},
NUMBER = {3},
PAGES = {483--498},
URL = {http://www.techscience.com/oncologie/v24n3/49719},
ISSN = {1765-2839},
ABSTRACT = {<b>Background:</b> Breast cancer (BC) is the most frequent type of gynecology tumors with high morbidity and mortality. Ampelopsin, the main active compound of <i>Ampelopsis grossedentata</i>, 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. <b>Materials and Methods:</b> 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. <b>Results:</b> In total, 25 potential target genes of ampelopsin were screened
out. The core target genes of ampelopsin against breast cancer were <i>AKT1</i>, <i>ESR1</i>, <i>ESR2</i>, <i>NCOA1</i>, <i>HSP90AA1</i>,
<i>NCOA2</i>, <i>BECN1</i>, <i>COMT</i>, <i>HMOX1</i>, and <i>CDK6</i>, 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. <b>Conclusions: </b>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.},
DOI = {10.32604/oncologie.2022.025148}
}