Evidence map›Paper›PMID 42198964›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2026

[Myricetin inhibits proliferation and migration of bladder cancer cells by inhibiting HSP90AA1-mediated AKT phosphorylation].

Ruixu Sun, Yutong Li, Ling Zuo, Jiahua Tao, Xuan Dong, Hongwei Liu

Abstract readEnglish Abstract
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 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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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Ruixu SunLaboratory of Urology, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China.
Yutong LiLaboratory of Urology, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China.
Ling ZuoDepartment of Traditional Chinese Medicine, Second Affiliated Hospital of Guangdong Medical University, Zhanjiang 524003, China.
Jiahua TaoLaboratory of Urology, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China.
Xuan DongLaboratory of Urology, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China.
Hongwei LiuLaboratory of Urology, Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo explore the targets and molecular mechanisms mediating the inhibitory effect of myricetin against bladder cancer.

methodsThe potential targets of myricetin were predicted using SwissTargetPrediction and SEA Search Server, bladder cancer-related targets were screened from TCGA transcriptome and FinnGen plasma proteome data, and the intersecting genes were obtained to identify the potential targets. A protein-protein interaction network was constructed, followed by GO and KEGG enrichment analyses. Molecular docking and dynamics simulations were performed to validate the binding between myricetin and the core targets. Amino acid residue virtual mutation was conducted to confirm the binding specificity of myricetin to HSP90AA1. Public single-cell transcriptomic and CRISPR screening data were analyzed to evaluate the cell-type specificity and functional essentiality of HSP90AA1. UM-UC-3 cells were used to examine the effects of myricetin on cell proliferation and migration and expressions of HSP90AA1 and PI3K-AKT pathway proteins.

resultsThirty potential targets of myricetin against bladder cancer were obtained, and HSP90AA1 was identified as the central target. KEGG analysis indicated significant enrichment of the target genes in the PI3K-AKT signaling pathway. Molecular docking and dynamics simulations demonstrated high binding affinity and stable conformation between myricetin and HSP90AA1. Bioinformatics analysis suggested that HSP90AA1 was highly and specifically expressed in bladder cancer urothelial cells, and its high expression was correlated with poor progression-free survival of the patients. In UM-UC-3 cells, myricetin concentration-dependently inhibited cell proliferation and migration, and downregulated mRNA level of HSP90AA1 and protein expressions of HSP90AA1, p-PI3K, and p-AKT.

conclusionsMyricetin inhibits bladder cancer cell proliferation and migration possibly by targeting HSP90AA1 and regulating the PI3K-AKT signaling pathway, suggesting its potential as a therapeutic agent for bladder cancer.

Indexed as

Cell MovementCell ProliferationFlavonoidsHSP90 Heat-Shock ProteinsProto-Oncogene Proteins c-aktUrinary Bladder NeoplasmsCell Line, TumorHumansMolecular Docking SimulationPhosphatidylinositol 3-KinasesPhosphorylationSignal TransductionFlavonoidsHSP90AA1 protein, humanHSP90 Heat-Shock ProteinsmyricetinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktbladder cancercomputational biologyCRISPR screenHSP90AA1myricetinsingle-cell transcriptomevirtual mutation

Identifiers

PMID42198964
PMCPMC13213344

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.