Mechanism of Quercetin in Inhibiting Triple-Negative Breast Cancer by Regulating T Cell-Related Targets: An Analysis Based on Single-Cell Sequencing and Network Pharmacology

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Hauptverfasser: Chen, Ruiqi, Hang, Liang, Wang, Fengyun
Format: Preprint
Veröffentlicht: 2025
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author Chen, Ruiqi
Hang, Liang
Wang, Fengyun
author_facet Chen, Ruiqi
Hang, Liang
Wang, Fengyun
contents Objective: To investigate the mechanism by which quercetin inhibits triple-negative breast cancer (TNBC) through regulating T-cell-related targets, providing a novel strategy for TNBC immunotherapy.Methods: Single-cell RNA sequencing (GSE161529 dataset) and network pharmacology were integrated. PCA and UMAP clustering identified T-cell subsets and differentially expressed genes in TNBC microenvironment. TNBC-related targets were screened via CTD and OMIM databases, with functional pathways analyzed by GO/KEGG enrichment. Molecular docking and PPI networks validated interactions between quercetin and core targets.Results: Quercetin intersected with 79 TNBC targets, including AKT1, EGFR, and MMP9, enriched in EGFR inhibitor resistance and endocrine resistance pathways. Molecular docking revealed the highest affinity between quercetin and GSK3B (-13.2 kJ/mol). AKT1 and MMP9 expression correlated with patient survival.Conclusion: Quercetin may reverse TNBC immunosuppression by multi-target modulation of T-cell function, but clinical application requires solutions for its low bioavailability, such as delivery systems or combination therapies.
format Preprint
id arxiv_https___arxiv_org_abs_2508_12731
institution arXiv
publishDate 2025
record_format arxiv
spellingShingle Mechanism of Quercetin in Inhibiting Triple-Negative Breast Cancer by Regulating T Cell-Related Targets: An Analysis Based on Single-Cell Sequencing and Network Pharmacology
Chen, Ruiqi
Hang, Liang
Wang, Fengyun
Molecular Networks
Genomics
Objective: To investigate the mechanism by which quercetin inhibits triple-negative breast cancer (TNBC) through regulating T-cell-related targets, providing a novel strategy for TNBC immunotherapy.Methods: Single-cell RNA sequencing (GSE161529 dataset) and network pharmacology were integrated. PCA and UMAP clustering identified T-cell subsets and differentially expressed genes in TNBC microenvironment. TNBC-related targets were screened via CTD and OMIM databases, with functional pathways analyzed by GO/KEGG enrichment. Molecular docking and PPI networks validated interactions between quercetin and core targets.Results: Quercetin intersected with 79 TNBC targets, including AKT1, EGFR, and MMP9, enriched in EGFR inhibitor resistance and endocrine resistance pathways. Molecular docking revealed the highest affinity between quercetin and GSK3B (-13.2 kJ/mol). AKT1 and MMP9 expression correlated with patient survival.Conclusion: Quercetin may reverse TNBC immunosuppression by multi-target modulation of T-cell function, but clinical application requires solutions for its low bioavailability, such as delivery systems or combination therapies.
title Mechanism of Quercetin in Inhibiting Triple-Negative Breast Cancer by Regulating T Cell-Related Targets: An Analysis Based on Single-Cell Sequencing and Network Pharmacology
topic Molecular Networks
Genomics
url https://arxiv.org/abs/2508.12731