Evidence map›Paper›PMID 40873180›Full record

ArticleAnti-cancer agents in medicinal chemistry2026

Ursolic Acid Inhibits Triple-Negative Breast Cancer Progression by Modulating the FGFR1/AKT/ERK Pathway: Evidence from Network Pharmacology and Experimental Validation.

Ziming Chen, Weiqiang Guo, Yahan Gao, Pu Zhao, Xin Liu, Min Qian, Shuhui You, Xiaoxiao Wang, Min Xiang

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Article in Anti-cancer agents in medicinal chemistry, 2026. 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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5 · Who and what money

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9 authors.

Ziming ChenSchool of Chemistry and Life Science, Suzhou University of Science and Technology, Suzhou, China.
Weiqiang GuoSchool of Chemistry and Life Science, Suzhou University of Science and Technology, Suzhou, China.
Yahan GaoSchool of Medicine, Suzhou Vocational Health College, Suzhou, China.
Pu ZhaoSchool of Chemistry and Life Science, Suzhou University of Science and Technology, Suzhou, China.
Xin LiuSchool of Chemistry and Life Science, Suzhou University of Science and Technology, Suzhou, China.
Min QianSchool of Chemistry and Life Science, Suzhou University of Science and Technology, Suzhou, China.
Shuhui YouSchool of Chemistry and Life Science, Suzhou University of Science and Technology, Suzhou, China.
Xiaoxiao WangSchool of Medicine, Suzhou Vocational Health College, Suzhou, China.
Min XiangSchool of Medicine, Suzhou Vocational Health College, Suzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionUrsolic acid (UA) exhibits antitumor activity; however, its effects and mechanisms on triple-negative breast cancer (TNBC) cells are not well understood. The present study aimed to explore the anti- TNBC mechanisms of UA by network pharmacology and experimental validation.

methodsTNBC cell lines MDA-MB-231 and BT-549 cells were treated with UA. A CCK-8 assay was performed to detect cell growth, while flow cytometry assessed cell cycle arrest and apoptosis. The underlying mechanism and potential targets of UA for TNBC treatment were investigated by network pharmacology, including PharmMapper database, GO, KEGG enrichment, and PPI analysis. The protein expressions and phosphorylation levels of FGFR1, AKT, and ERK were measured by western blot. Pull-down assay, cellular thermal shift assay (CETSA), and molecular docking were used to analyze the interaction between UA and FGFR1. Xenograft models were established to examine the effect of UA on TNBC tumor growth.

resultsUA effectively reduced cell viability, induced apoptosis, and arrested cell cycle in TNBC cells. Moreover, UA significantly regulated the expression of Bcl-2 and Bax to induce apoptosis. The results of network pharmacology and western blot suggested that UA reduced FGFR1/AKT/ERK pathway. Furthermore, pull-down, CETSA, and molecular docking results revealed that UA directly bound to FGFR1. In the xenograft model, UA inhibited the growth by suppressing FGFR1. DISCUSSION: In this study, we employed network pharmacology and experimental approaches to elucidate the mechanism of UA on TNBC. The results demonstrated that UA targeted FGFR1 to inhibit TNBC via mediating FGFR1/AKT/ERK pathway.

conclusionsOur findings demonstrate that UA inhibits the FGFR1/AKT/ERK pathway by directly targeting FGFR1, thereby suppressing TNBC progression and supporting its potential as a therapeutic agent for TNBC treatment.

Indexed as

Antineoplastic Agents, PhytogenicProto-Oncogene Proteins c-aktReceptor, Fibroblast Growth Factor, Type 1Triple Negative Breast NeoplasmsTriterpenesAnimalsApoptosisCell ProliferationCell SurvivalDose-Response Relationship, DrugDrug Screening Assays, AntitumorExtracellular Signal-Regulated MAP KinasesFemaleHumansMiceMice, NudeAntineoplastic Agents, PhytogenicExtracellular Signal-Regulated MAP KinasesFGFR1 protein, humanProto-Oncogene Proteins c-aktReceptor, Fibroblast Growth Factor, Type 1TriterpenesUrsolic Acidapoptosiscell cyclefgfr1/akt/erk pathwaynetwork pharmacologytriple-negative breast cancerUrsolic acid

Identifiers

PMID40873180

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