Evidence map›Paper›PMID 41021160›Full record

ArticleDiscover oncology2025

Mechanistic evaluation of hyperoside against non-small cell lung cancer: a combined approach of network pharmacology and in vitro experimental validation.

Shuang Xu, Yaping Zou, Guangwen Luo, Liu Tang, Haichao Zhan, Lili Huang, Zhaowei Zhang

Abstract read
In one paragraph

Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Shuang Xu *Department of pharmacy, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, 321000, Zhejiang, China.
Yaping Zou *Department of Otorhinolaryngology, Head and Neck, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, 321000, China.
Guangwen LuoDepartment of pharmacy, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, 321000, Zhejiang, China. lgw2018@126.com.
Liu TangDepartment of pharmacy, Renmin Hospital of Wuhan University, Wuhan, 430060, Hubei, China. tangliu900402@whu.edu.cn.
Haichao ZhanDepartment of pharmacy, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, 321000, Zhejiang, China.
Lili HuangDepartment of pharmacy, Ningbo Medical Center Lihuili Hospital, Ningbo, 315040, China.
Zhaowei ZhangDepartment of pharmacy, Affiliated Jinhua Hospital, Zhejiang University School of Medicine, Jinhua, 321000, Zhejiang, China.

Funding

Initial Scientific Research Foundation for Affiliated Jinhua Hospital, Zhejiang University School of Medicine JY2019-2-01Jinhua Traditional Chinese Medicine Science and Technology Plan Project 2025LC04
6 · The paper itself

Abstract

backgroundHyperoside (Hyp) exerts considerable inhibitory effects on non-small-cell lung cancer (NSCLC) cells. However, the underlying molecular mechanisms have not been fully elucidated. We aimed to explore the molecular mechanisms of Hyp in the treatment of NSCLC using a combination of network pharmacology and in vitro experiments.

methodsActive targets of Hyp and NSCLC-related targets were identified using public databases. The therapeutic targets were predicted based on the intersection of drug and disease targets. A protein-protein interaction (PPI) network was constructed using STRING and Cytoscape, and key network modules and targets were identified through network topology analysis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using DAVID. Molecular docking between Hyp and therapeutic targets was performed using AutoDock Vina software. These results were further verified by in vitro experiments of A549 cell lines, including the CCK-8 assay, EdU staining, flow cytometry and western blotting.

resultsA total of 30 therapeutic targets of Hyp against NSCLC were identified. Analysis of the PPI network revealed a key network module and five key targets: MMP9, CASP3, MAPK1, ESR1, and EGFR. These targets were related to cell proliferation and migration, apoptosis, and oxidative stress and may play a role through the FoxO, MAPK, Rap1, Ras, and PI3K-Akt signaling pathways. Molecular docking results showed a strong binding affinity between Hyp and most therapeutic targets. Further experiments confirmed that Hyp inhibited proliferation and induced apoptosis of A549 cells by regulating the EGFR/ERK/FOXO1 signaling pathway.

conclusionsHyp may be a promising drug for treating NSCLC (especially lung adenocarcinoma), and its therapeutic mechanisms is closely related to the regulation of EGFR/ERK/FOXO1 pathway.

Indexed as

ApoptosisEGFR/ERK/FOXO1 pathwayHyperosideNetwork pharmacologyNon-small-cell lung cancer

Identifiers

PMID41021160
PMCPMC12480148

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