Discovery and Target Verification of Active Ingredients of Nostoc Commune in Anti-triple-negative Breast Cancer
10.13748/j.cnki.issn1007-7693.20221152
- VernacularTitle:地皮菜抗三阴性乳腺癌作用活性成分的发现与靶点验证
- Author:
FAN Miaozhen
1
;
LUO Zhenhua
1
;
WANG Huideng
1
;
WANG Yuhui
1
;
DUAN Xiaoqun
1
;
XU Xiaotian
1
Author Information
1. School of Pharmacy, Guilin Medical University, Guilin 541199, China
- Publication Type:Journal Article
- Keywords:
Nostoc commune;
triple-negative breast cancer;
network pharmacology;
molecular docking;
AKT1
- From:
Chinese Journal of Modern Applied Pharmacy
2023;40(18):2484-2491
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To explore the mechanism of action of active components of Nostoc commune in anti-triple-negative breast cancer(TNBC) by the network pharmacology method and molecular biology experiment. METHODS The active components of Nostoc commune were collected by consulting the literature and combined with the preliminary research in the laboratory, the Swiss Target Prediction database was used for target prediction, and the disease targets were obtained in the TTD, Genecards and OMIM databases. The STRING online platform was used for protein-protein interaction, and the KEGG signaling pathway and GO gene function enrichment analysis were performed using the Metascape database. Molecular docking of N-acetyltryptamine, a component of Nostoc commune, and target AKT1 by AutoDock software. Annexin V-FITC/PI double staining method was performed to analyze the apoptotic rate of cells. RT-qPCR and Western blotting were used to detect the mechanism of action of the active components of Nostoc commune on anti-TNBC. RESULTS The results of network pharmacology showed that there were 8 effective components, such as N-acetyltryptamine, Scytonemin and Nostocionone, involved 75 key targets such as signal transduction and AKT1, STAT3 and CCND1. The KEGG signaling pathway and GO gene function enrichment analysis results involved cancer-related signaling pathways, PI3K-Akt signaling pathways and MAPK signaling pathways. Molecular docking showed that N-acetyltryptamine had better affinity with AKT1. N-acetyltryptamine could not significantly promote apoptosis of breast cancer cells. Western blotting showed that N-acetyltryptamine could down-regulate the protein expressions of AKT1. The results of RT-qPCR showed that N-acetyltryptamine could effectively reduce the mRNA expression of AKT1 in cells. CONCLUSION N-acetyltryptamine may inhibit the proliferation of TNBC cells by inhibiting the AKT1 signaling pathway, thereby exerting anti-TNBC effects.
